AMC Anthology of Medical Conditions - Unlocked

001 Abdominal Distension/Ileus (Ascites, Bowel
Obstruction)
Overview
Abdominal distension is common and may indicate the presence of serious intra-
abdominal or systemic disease. Clinically, distension is separable into two main types
of presentation: Acute distension (usually painful and predominantly surgical) , or
Chronic/ Subacute distension (usually painless and associated with obstetrical/
gynaecological and medical causes) . Remember all the 'Fs. which cover many of the
causes over both groups: Fluid, Flatu s. Faeces, Fat, Fetus, large Focal masses. and
the False impressions of pseudopregnancy.
Causes
j 1) Acute abdominal distension

a} Mechanical intestinal ob struction (luminal, wall , extrinsic- usually
painful}
The most common causes are adhesions, tumours , hernias, volvul us
U Gastric outlet obstruction - ·pyloric' stenosis
u Small intestine - adhesions. hernias, tumours etc.
U Large intestine - tumours , diverticular disease, volvu lus
Abdominal distension- pyloric stenosis (adult)
b) Non-mechanical intestinal obstruction

(acute intestinal pseudo-obstruction- sometimes painless}
.J Acute gastric dilatation
U Small and large intestine - 'paralytic' or 'spastic' ileus
• Transient postoperative physiological ileus
• Secondary to peritonitis from any cause
• Secondary to ischaemia (mesenteric infarction. ischaemic enteritis)
• Toxic inflammatory bowel disease (I BD) (toxic megacolon)
• Secondary to severe systemic illness or retroperitoneal pathology
(haemorrhage, tumours. etc.)
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2) Chronic abdominal distension (usually painless)
a) Ascites
b) Faecal impaction
c) Large abdominal or pelvic mass
0 Hepatosplenomegaly
0 Neoplasms
0 Abdominal aneurysms
0 Ovarian cysts
0 Gross bladder distension
d) Pregnancy (exclude first in females)
e) Subjective (false pregnancy, irritable bowel syndrome, obesity)
Abdominal distension - ascites
3) Chronic nonmechanical intestinal pseudo-obstruction

a) Enteric nervous system (amyloidosis, diabetes, paraneoplastic)
b) Extrinsic nervous system (stroke, spinal cord injury, multiple sclerosis
Parkinson disease, autonomic dysfunction)
c) Smooth muscle (scleroderma)
30
Key Objectives
• Differentiate between causes of abdominal distension based on history and
physical findings.
• Identify causes of acute abdominal distension requiring urgent early care.
General/Specific Objectives
• Through efficient, focused data gathering:
Differentiate clinically the aetiology of abdominal distension.
Elicit information on risk factors which would predispose to the various
causes for abdominal distension.
• Interpret the critical clinical and laboratory findings which were key in the
processes of exclusion, djfferentiation and diagnosis:
Select and interpret abdominal X-rays and other appropriate investigations
used in cases of abdominal distension.
Recommend paracentesis when indicated and interpret the results.
• Conduct an effective plan of management for a patient with abdominal
distension/ileus:
Outline the short term medical and surgical management of patients with
gaseous distension.
Contrast the immediate and long term management of a patient with
cirrhotic ascites versus malignant ascites.
Select patients in need of specialised care.
Abdominal distension -
ovarian cyst
31
002 Abdominal Mass
Overview
Most abdominal masses represent significant underlying disease requiring complete
investigation. Intra-abdominal masses must be differentiated from abdominal wall
masses. The large number of possible causes can be made more manageable by
focusing on the site and physical characteristics of the mass. (See #002A Epigastric
Mass - #002F Left Iliac Fossa Mass.)
Causes
1) Organomegaly
a) Hepatomegaly
b) Splenomegaly
c) Enlarged kidneys
d) Retroperitoneal masses
12) Gastrointestinal system masses

a) Gastric, colonic, appendiceal
b) Stool
c) Pancreatic (pseudocyst)
d) Gallbladder mass
3) Vascular (abdominal aortic aneurysm)
14) Gynaecologic J Pelvic Retroperitoneal liposarcoma

a) Pregnant uterus
b) Ovarian mass
c) Enlarged bladder
I 5) Lymphadenopathy
a) Lymphomas
b) Metastases
c) Infectious causes
I6) Masses in abdominal wall

(see #002G Abdominal Hernia)
a) Rectus sheath haematoma
b) Desmoid tumour
c) Umbilicallump/discharge
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0 Intertrigo, concretions , granulomas
0 Malignant nodule (Sister Mary Joseph nodule)
0 Pilonidal sinus
0 Endometriosis
0 Embryological remnants (vitelline duct, urachus)
Key Objectives
• Distinguish the cause of an abdominal mass based on history and physical
findings.
• Distinguish intra-abdominal from abdominal wall masses .
. .nerai/Specific Objectives
Exclude pregnancy as cause of the abdominal mass.
Determine which patients are likely to have a neoplasm causing the
abdominal mass.
Determine the physical characteristics enabling diagnosis of masses arising
in specific organs.
Describe the risk factors which would predispose to the various causes
for abdominal mass.
• Interpret critical clinical and laboratory findings which were key in the processes
of exclusion, differentiation and diagnosis:
Select and interpret abdominal imaging (radiography, computed
tomography (CT) scan, ultrasound, etc.) in patients with an abdominal
mass.
Interpret and discuss the role of serum tumour marker testing .
• Conduct an effective plan of management for a patient with an abdominal
mass:
Discuss the medical and surgical management of patients with an
abdominal mass.
33
002 Abdominal Mass ·
002A Epigastric Mass
Overview
Epigastric masses are most commonly due to pathology in stomach or liver; or may
indicate retroperitoneal pathology (aneurysm, pancreatic or lymph node mass).
Causes
11) Abdominal aortic aneurysm
2) Gastric mass (neoplasm, gastric dilatation)
13) Liver mass (left lobe)
4) Pancreatic mass (pseudocyst, tumour)
Is) Lymph node mass (para-aortic nodes)
Key Objective
• Distinguish the cause of an epigastric mass based on history and physical
findings.
Identify site of origin and likely cause of an epigastric mass based on
clinical findings.
• Interpret the critical clinical and laboratory findings in diagnosis.
• Outline an effective management plan for a patient with an epigastric mass.
Aortic aneurysm
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002 Abdominal Mass
0028 Right Hypochondria/ Mass
Overview
Masses in the right hypochondrium arise most commonly from the liver or gallbladder.
The normal liver is impalpable, except in children. The liver becomes palpable when
abnormally firm and enlarged or when it contains a mass.
Causes
11) Hepatomegaly
a) General enlargement
(J Cirrhosis
0 Heart failure
b) Focal masses
0 Neoplasms, parasitic cysts , etc.
12) Enlarged gallbladder

a) Acute cholecystitis
b) Mucocele I Empyema
c) Courvoisier sign and law (underlying pancreatic neoplasm)
13) Hepatic flexure colonic mass
14) Right renal mass
Daughter cysts In hepatic hydatid
35
Key Objective
• Distinguish the cause of a right hypochondria! mass based on history and
physical findings.
Identify site of origin and likely cause of a right hypochondria! mass.
of exclusion, differentiation and diagnosis.
• Outline an effective diagnostic/management plan for a patient with a right
hypochondria! mass.
• Outline the management of a patient presenting with a mass due to acute
cholecystitis.
• Outline the management of a patient with a mass in the liver due to a hydatid
cyst:
Describe the life cycle of the hydatid parasite through definitive (primary)
and intermediate host cycles; describe the types of clinical presentation
and methods of diagnosis and treatment of hydatid cyst disease in humans.
Primary hepatocellular carcinoma
36
002 Abdominal Mass
002C Left Hypochondria/ Mass
Overview
Masses in the left hypochondrium are most commonly caused by splenic enlargement,
which must be differentiated from renal, colonic or pancreatic tail lesions.
Causes
1) Splenomegaly
2) Left renal mass
3) Colonic mass (splenic flexure)
4) Pancreatic tail mass
Key Objective
• Distinguish the cause of a left hypochondria! mass based on history and
physical findings.
Differentiate splenic from other masses.
• Outline an effective management plan in a patient with a left hypochondria!
mass due to splenomegaly.
• Outline effective diagnostic and management plans in patients with a left renal
mass.
Wilms tumour
37
002 Abdominal Mass
0020 Right Iliac Fossa Mass
Overview
Painful right iliac fossa masses commonly are associated with appendiceal or colonic
pathology and require prompt surgical assessment.
Causes
1) Appe ndiceal mass
{phlegmon or abscess)
12) Caecal mass (carcinoma)
3) Other infectious/inflammatory
causes
a) Crohn disease
b) Actinomycosis
c) lleocaecal tuberculosis (TB)
d) Psoas abscess
14) Iliac lymph node swellings

a) Lymphoma
b) Metastatic
Key Objective
• Distinguish the cause of a right iliac fossa mass based on history and physical
findings.
• Outline a management plan for a patient presenting with a right iliac fossa
mass.
• Select and interpret imaging investigations (radiography, computed
tomography (CT) scans, ultrasound, etc.) in patients presenting with a right
iliac fossa mass.
38
002 Abdominal Mass
002E Suprapubic/Pelvic Mass
Overview
In women a pregnant uterus must first be excluded. Other gynaecologic causes include
large ovarian or uterine abdomi nopelvic masses. In both sexes, a distended bladder is
an important cause.
Causes
11) Pregnant uterus
I 2) Urinary bladder
I 3) Ovarian mass
Key Objective
• Distinguish the cause of a suprapubic mass on the basis of history and physical
findings.
General/Specific Objective
• Outline effective diagnostic/management plans for a patient with a suprapubic
mass.
Suprapubic/pelvic mass - ovarian cyst
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002 Abdominal Mass
002F Left Iliac Fossa Mass
Overview
let\ mac tossa masses are mos\ commonly due to significant colonic pathology.
Causes
1) Colonic mass
a) Carcinoma sigmoid colon
b) Colonic diverticular disease
c) Faeces
I 2) Lymph node mass
Key Objective
• Distinguish the cause of a left iliac fossa mass based on history and physical
findings.
• Outline effective diagnostic/management plans for a patient with a left iliac
fossa mass.
• Outline the diagnostic plans for a patient presenting with left iliac fossa mass
due to iliac lymph node enlargement.
Diverticular disease
40
002 Abdominal Mass
002G Abdominal Hernia
Overview
Herniorrhaphy is the commonest surgical procedure performed by general surgeons.
Twenty-five per cent of males will develop an inguinal hernia in their lifetime. Interference
with the blood supply of the hernial contents (strangulation) is a surgical emergency.
Causes
l1) Groin hernias

a) Inguinal hernia (direct, indirect)
0 Commoner in males
b) Femoral hernia
0 Commoner in females
I2) Umbilical hernias

a) Congenital umbilical hernia of infancy
0 Most settle spontaneously
b) Adult umbilical/para-umbilical hernia
0 Multiparity in females major causal
factor
13) lncisional (wound) hernia

Indirect inguinoscrotal
a) Commoner with vertical incisions inguinal hernia
b) Wound infection commonest cause
14) Less common abdominal wall hernias!

a) Epigastric hernia (fatty hernia of linea alba)
b) Spigelian (linea semilunaris) hernia
0 Characteristically interstitial
c) Lumbar hernia
d) Perineal hernia (usually after
abdomino-perineal excision
of rectum)
Bilateral inguinal hernias
41
5) Divarication of recti
a) Diffuse epigastric bulge between recti in epigastrium due to obesity

and spreading of linea alba - not a true hernia
6) Internal abdominal hernias
Femoral hernia
Para-umbilical hernia
Key Objectives
• Identify abdominal wall hernias requiring immediate rather than elective repair.
• Recognise factors predictive of hernia recurrence postoperatively (such as
wound sepsis, obesity, ascites and malnutrition).
Recognise symptoms and signs of strangulated hernia, as opposed to
irreducibility.
Differentiate inguinal and femoral hernias from other causes of a groin (or
inguinoscrotal) mass such as lymphadenopathy, varicocele , hydrocele,
saphena varix or femoral aneurysm.
Differentiate inguinal from femoral hernia on the basis of physical signs
including visual inspection, palpation and special manoeuvres.
• Conduct an effective diagnostic and management plan for a patient with an
abdominal wall hernia:
Identify patients in need of surgical repair (emergency and elective).
Identify factors predisposing to abdominal wall hernia.
Counsel and educate patients on the risks associated with uncorrected
hernias and identify hernias at special risk of strangulation.
Identify possible sites of intra-abdominal herniation by considering
embryology of intra-abdominal structures; and outline the potential clinical
significance of intra-abdominal hernias.
42
002 Abdominal Mass
002H Adrenal Mass
Overview
Adrenal masses are at times found incidentally after computed tomography (CT) scan,
magnetic resonance imaging (MRI), or ultrasound examination done for unrelated
reasons . The incidence is about 3% {almost 10% of autopsies). Larger masses are
likely to require investigation. Functioning adrenal masses comprise a group causing
important treatable causes of hypertension.
Causes
11) Non-functioning ade noma
I2) Functioning ade noma

a) Cushing syndrome (glucocorticoid excess)
b) Conn syndrome (aldosterone excess)
c) Androgen excess
d) Phaeochromocytoma
I 3) Adrenal carcinoma
I 4) M etastasis
I 5) Ne uroblastoma (in children) I
Adrenal neuroblastoma
Serum I Plasma
Sodium 139 mmoi/L
Potassium .!]. 2.4 mmoi/L
Chloride 96 mmoi/L
Bicarbonate fr' 34 mmoi/L
Urea 3.8 mmoi/L
Creatinine 71 p moi/L
Ionised calcium v 1.11 mmoi/L
Aldosterone 2029 pmoi/L
Renin <7.0 mUlL
Adrenal mass on CT, with serum chemistry - Conn syndrome
43
Key Objectives
• Determine whether the mass is malignant or not.
• Determine whether the mass is functional or not.
Differentiate benign functioning adenomas from those that are non-
functioning .
Differentiate benign from malignant masses by inquiring and examining
for primary tumours which metastasise to the adrenal glands.
of exclusion, differentiation, and diagnosis:
Select and interpret investigations for the exclusion of functioning adrenal
masses.
List features noted on diagnostic imaging techniques suggestive of
malignancy.
Select patients and list indications for fine needle aspiration cytological
(FNAC) biopsy.
• Conduct an effective plan of management for a patient with an adrenal mass:
Outline initial plan of management for patients with adrenal masses which
are functioning.
• Select patients in need of specialised care; list those requiring referral to
endocrinology I internal medicine, and those requiring surgical referral.
44
' --
003 Abdominal Pain
- - -
003A Abdominal Pain in Adults
Overview
Abdominal pain may result from intra-abdominal inflammation or disorders of the
abdominal wall. Pain may also be referred from sources outside the abdomen such as
retro-peritoneal processes as well as intrathoracic processes. Thorough clinical
evaluation is the most important 'test' in the diagnosis of acute abdominal pain.
Localisation of the pain site, and awareness of characteristic symptom sequences, can
reduce the list of possible causes to manageable size.
Causes
1) Right upper quadrant pain
a) Biliary tract
l.J Biliary 'colic'
0 Acute cholecystitis
Cl Cholangitis
b) Liver (hepatitis, hepatic
abscess, neoplasms)
c) Pancreatiti s
d) Renal pain (pyelonephritis,
tumours, infarction and Acute cholecystitis
polycystic kidney)
e) Extra-abdominal (myocardial infarction (MI), pulmonary embolus,
pneumonia)
I 2) Epigastric pain
a) Peptic ulcer disease
b) Pancreatitis
c) Cholangitis
d) Functional dyspepsia
e) Neoplasms (hepatic, gastric, pancreatic)
f) Abdominal aortic aneurysm
g) Epigastric hernia
I 3) Left upper quadrant pain

b) Pancreatitis
c) Gastric and pancreatic neoplasms
d) Renal pain
14) Right/Left lower quadrant pain I
a) Bowel (appendicitis, colitis,
diverticulitis: large and small
bowel)
b) Mesenteric lymphadenitis
c) Gynaecologic causes
(complicated ovarian cyst,
ectopic pregnancy, pelvic
inflammatory disease)
d) Ureteric/Renal 'colic'
e) Urinary retention
f) Pyelonephritis and cystitis Ureteric calculus - renal 'colic'
I 5) Generalised
a) Functional gut disorders (functional
dyspepsia, irritable bowel syndrome)
b) Peritoneal inflammation (ruptured
viscus, bacterial peritonitis)
c) Bowel obstruction
d) Vascular (ischaemic bowel, ruptured
abdominal aortic aneurysm)
e) Metabolic (diabetic ketoacidosis,
porphyria)
f) Neurogenic (herpes zoster)
g) Other (Mediterranean/Malta fever Small bowel obstruction -
adhesions
(brucellosis), sickle cell crisis, etc.)
6) Special group 'acute abdomen - acute abdominal surgical

emergency'
a) Perforated viscus (peptic ulcer,
appendix, gallbladder, colon)
Perforated peptic ulcer
0 Perforated appendicitis I cholecystis
0 Perforated colonic diverticulitis with
faecal peritonitis
b) Strangulated intestinal obstruction
c) Ruptured aortic aneurysm
d) Acute haemorrhagic pancreatitis
(pancreatic necrosis)
e) Ruptured ectopic pregnancy
f) Acute massive mesenteric vascular infarction
46
g) Blunt or penetrating trauma with peritonitis
h) Primary bacterial peritonitis
Perforated colonic diverticulitis Intestinal obstruction - stangulated

groin hernia
Key Objectives
• Recognise patients with abdominal pain who requ ire emergency treatment,
medical or surgical.
• Recognise the special group of 'acute abdomen - acute abdominal surgical
emergency' where early surgical referral and exploration is likely to be required.
• Determine whether extra-abdominal causes listed above (MI, etc.) may be
causing the pain.
Elicit clinical findings and their sequence which are key to establishing the
most likely source of the pain.
Differentiate intra-abdominal from extra-abdominal or metabolic causes
of acute abdominal pain.
processes of exclusion, differentiation and diagnosis:
Interpret abdominal X-rays and other imaging modalities diagnostic of
various causes .
• Conduct an effective plan of management for a patient with acute abdominal
pain:
Select patients who require emergency surgery and who require emergency
medical care .
Outline a plan of management for common causes of abdominal pain.
Select patients in need of specialised care and/or further investigation.
Understand the common and life-threatening causes of acute abdominal
pain.
47
003 Abdominal Pain
0038 Non-Acute/Recurrent Abdominal Pain in Infancy

and Early Childhood
Overview
Abdominal pain is a common and disconcerting problem in infants and children. In an
infant or child presenting with chronic but persistent intermittent abdominal pain, the
probable causes should be rapidly identified so that directed management can be
initiated. Causes of acute abdominal pain are considered in #003F Acute Abdominal
Pain in Children.
Causes
j 11 Organic
a) Abdominal
Infantile colic
0 Infectious (Giardia Iamblia)
0 Obstructive (chronic constipation)
0 Trauma
Vasculitic
Miscellaneous
b) Extra-abdominal
Miscellaneous (peptic ulceration, intermittent porphyria)
I 2) Functional
a) Psychogenic (family disruption, school failure)
Key Objective
• It is important to differentiate between functional and organic causes and to
recognise how causes of abdominal pain in infants and children differ from
those in adulthood.
In an infant, identify the acute organic causes and differentiate from infantile
colic.
Differentiate acute from chronic and functional abdominal pain.
Select appropriate laboratory investigations to differentiate those conditions
requiring acute management.
48
Investigate colic and functional pain with the minimum investigations to
establish the diagnosis.
Identity from investigations, the key essentials differentiating acute from
chronic pain.
• Conduct an effective plan of management for a patient with abdominal pain:
In infants, outline the initial stages for management of acute intestinal
obstruction.
Manage infantile colic with the infant's interests as the focus.
Manage functional abdominal pain with the child's interests as the focus.
Outline the treatment programme for a child with chronic abdominal pain
utilising the support of the parents, family and community services.
49
003 Abdominal Pain
003C Chronic Recurrent Abdominal Pain
Overview
Chronic and recurrent abdominal pain is a common symptom with an extensive
differential diagnosis and heterogeneous pathophysiology. The history and physical
examination frequently differentiate between functional and more serious underlying
diseases.
Causes
1) Intestinal tract
a) Oesophageal (oesophagitis)
b) Gastric (peptic ulcer disease, neoplasm)
c) Duodenal (peptic ulcer disease)
d) Small bowel (inflammatory bowel disease (lBO), neoplasm)
e) Colon (lBO, irritable bowel syndrome, neoplasm, diverticulosis)
I2) Relat ed organs

a) Gallbladder I Biliary tract (cholelithiasis I biliary 'colic')
b) Pancreas (chronic pancreatitis, neoplasm)
Bile duct stone - MRCP and ERCP
50
J3) Other
a) Psychogenic factors (malingering, functional dyspepsia)
b) Abdominal wall
c) Gynaecologic causes
d) Visceral neoplasms/lymphomas
e) Collagen I Vascular
f) Lactose intolerance
Key Objective
• Recognising that visceral pain is typically poorly localised and often referred
to distal sites, differentiate between various causes of chronic abdominal pain.
Differentiate between organic and non-organic causes of chronic abdominal
pain.
Select patients in need of further laboratory and radiological investigation.
Outline the significance of common findings on ultrasound or computed
tomography (CT) imaging of the abdomen as well as barium contrast
studies.
• Conduct an effective plan of management for a patient with chronic abdominal
pain:
Contrast the medical, surgical, nutritional and psychological management
of chronic abdominal pain.
Select narcotics appropriately for patients and manage complications
arising from the use of these drugs.
Select patients in need of referral to other healthcare professionals.
Counsel and provide appropriate education for patients with chronic
abdominal pain syndromes.
51
003 Abdominal Pain
0030 Heartburn/Dyspepsia
Overview
'Heartburn' and 'dyspepsia' are common gastrointestinal complaints, since studies from
various countries report an incidence of the symptoms in 20-40% of adults. Although
serious complications can arise with few premonitory symptoms, appropriate
management can generally avert such sequelae.
Causes
1) Functional dyspepsia I Somatof orm disorders
2) Gastro-oesophageal reflux disease with/without oesophagitis
I3) Motility disorders of the oesophagus

a) Achalasia
b) Scleroderma
4) Peptic ulcer disease (including drugs)
5) Miscellaneous (biliary disease, irritable bowel, chronic

pancreatitis, diabetic gastroparesis, ischaemic heart disease,
etc.)
Key Objectives
• Diagnose somatoform disorders by inclusion rather than exclusion ; always
exclude the possibility of ischaemic heart disease.
• Outline conservative management measures including dietary counselling.
Differentiate between dyspepsia and chest pain or referred pain resulting
from ischaemic heart disease.
List or outline indications for radiological or endoscopic investigation of
patients with symptoms suggestive of gastro-oesophageal reflux or peptic
ulcer.
• Conduct an effective plan of management for a patient with 'heartburn':
Discuss the current concepts of pathophysiology in the management of
gastro-oesophageal reflux and peptic ulcer disease.
52
Counsel patients regarding lifestyle modification which can ameliorate
symptoms of gastro-oesophageal reflux and peptic ulcer disease.
Select patients in need of specialised care .
Oesophageal motility disorder
Sliding oesophageal hiatus hernia
53
003 Abdominal Pain
003E Anal Pain
Overview
While almost all causes of anal pain are
treatable, some can be destructive locally if left
untreated. Anal pain is not a feature of
uncomplicated haemorrnoias.
Causes
1) Identifiable
a) Perianal haematoma
b) Haemorrhoids (painful due to
thrombosis, infection, or erosion)
c) Anal fissure
d) Anal ulcer I Anal cancer
e) Perianal fistula (due to Crohn
disease)
Acute perianal haematoma
f) Perirectal abscess
j2) Other
a) Proctalgia fugax, neuropathic
pain syndrome
b) Coccygeal pain, other pelvic
floor muscle syndromes
Anal fissure
54
Key Objective
• Perform visual inspection, palpation, and ano-rectal examination in all patients
presenting with anal pain.
Differentiate between the causes of anal pain.
Establish whether tenesmus (an uncomfortable sense of incomplete
evacuation leading to frequent, painful straining) is present.
Based on inspection, palpation and ano-rectal examination, differentiate
the cause of anal pain.
• Conduct an effective plan of management for a patient with anal pain:
Select patients with perirectal abscess for urgent surgical treatment.
Counsel patients with haemorrhoids and anal fissure in the conservative
treatment options including sitz baths, stool softeners and secondary
preventive measures such as strict avoidance of constipation.
Anal fistula
55
003 Abdominal Pain
003F Acute Abdominal Pain in Children
Overview
Acute abdominal pain in children may result from intra-abdominal inflammation or
obstruction. Thorough clinical evaluation is usually the most important step in the
diagnosis of abdominal pain so that directed management can be initiated.
Causes
1) Right lower quadrant I Left lower quadrant
a) Appendicitis, constipation
b) Mesenteric lymphadenitis
c) Inflammatory bowel disease (lBO)
d) Inguinal hernia (incarcerated)
I 2) Generalised
a) Peritoneal inflammation (ruptured viscus, bacterial peritonitis)
b) Bowel (infantile colic, gastroenteritis, bowel obstruction
(intussusception, constipation))
c) Psychosomatic
d) Extra-abdominal (referred pain - pneumonia)
Key Objective
• Select pat1ents with abdominal pain who require emergency treatment, medical
or surg1cal.
Elicit clinical findings which are key to establishing the most likely source
of the pain.
of exclusion. differentiation, and diagnosis:
Select laboratory and diagnostic imaging, where appropriate, to determine
whether cond1t1ons requiring emergency treatment are present.
Interpret abdominal X-rays.
• Conduct an effective plan of management for children with acute abdominal
pain:
Select patients who require emergency surgery and those who require
emergency medical care.
56
Outline the initial plan of management in infants with acute intestinal
obstruction.
Outline a plan of management for common causes of abdominal pain
(e.g. infantile colic) with the child's interest as the focus.
Outline a plan of management for a child with acute abdominal pain
using support from parents, family, and community services.
Select patients in need of specialised care and/or further investigation.
Inguinal hernia - non-reducible Ileocolic intussusception
57
004 Abnormal Serum Calcium/Phosphate
004A Hypercalcaemia
Overview
Hypercalcaemia may be associated with an excess of calcium in both extracellular
fluid and bone (e.g. increased intestinal absorption), or with a localised or generalised
deficit of calcium in bone (e.g. increased bone resorption). This differentiation is
important for both diagnostic and management reasons . Hypercalcaemia in adults
requires investigation to identify the cause. Primary hyperparathyroidism (HPT) is a
common cause and is differentiated from other causes such as bone malignancy by
high serum parathormone.
Most patients with hypercalcaemia due to primary HPT have or will develop symptoms,
the most important of which are changes in the mental state) lethargy, constipation,
thirst, urinary frequency and nocturia. Surgery is indicated in the majority of patients
with established primary HPT- the commonest cause is a single parathyroid adenoma.
Hypercalcaemia can cause severe anatomic injury to the kidneys and, if severe, patients
may develop hypercalcaemic crisis.
Causes
1) Increased bone resorption
a) Malignancy
b) Primary HPT
c) Secondary/Tertiary HPT
d) Hyperthyroidism
e) 1m mobilisation
f) Paget disease of bone
I2) Increased intestinal absorption

a) Increased intake (e.g. milk alkali syndrome)
b) Vitamin 0-mediated (e.g. granulomatous diseases such as sarcoidosis)
3) Diminished excretion (familial hypocalciuric

hypercalcaemia, drugs)
I4) Miscellaneous
58
Parathyroid adenoma
Key Objective
• Formulate a management plan for hypercalcaemia consistent with its causal
conditions.
Outline a diagnostic and management plan for a patient with
hypercalcaemia.
Outline laboratory tests and diagnostic imaging findings in relation to the
common causes and contrast the findings in primary HPT, secondary HPT,
cancer and Paget disease.
Outline embryological development of parathyroids and the relevance to
sites of parathyroid adenomas.
Differentiate hypercalcaemia caused by increased intake from that of
excess bone resorption.
processes of exclusion, differentiation and diagnosis.
• Conduct an effective plan of management for a patient with hypercalcaemia:
59
0048 Hypocalcaemia
Over view
Hypocalcaemia is an important and potentially serious complication from a variety of
causes. Tetany, seizures, and papilloedema may occur in patients who develop acute
hypocalcaemia. Early recognition of symptoms of paraesthesiae is important in
diagnosis and treatment in order to prevent these complications in patients at risk.
Causes
1) Loss of calcium from the circulation
a) Hyperphosphataemia (renal insufficiency)
b) Pancreatitis
c) Osteoblastic metastases
d) Drugs (ethylenediamine tetra-acetic acid (EDTA), citrate)
e) Rhabdomyolysis
f) Respiratory (overbreathing) or metabolic alkalosis
2) Decreased vitamin D production or action

a) Renal fa ilure
b) Rickets/Rachitis
c) Malabsorption
3) Decreased parathyroid hormone (PTH) production or actions

a) After thyroid/parathyroid surgery
b) Autoimmune
c) Diminished response
I 4) Hypomagnesaemia
60
Key Objectives
• Early recognition and treatment of hypocalcaemia in patients at risk.
• Calculate a corrected calcium concentration in the presence of
hypoalbuminaemia before initiating any other investigation.
Differentiate hypocalcaemia caused by hyperphosphataemia/
hypomagnesaemia from that of diminished production or action of PTH
or vitamin D.
Contrast laboratory findings in the various conditions causing
hypocalcaemia.
• Conduct an effective plan of management for a patient with hypocalcaemia:
Formulate a management plan for acute hypocalcaemia associated with
either tetany or seizures.
61
004C Hypophosphataemia I Fanconi Syndrome
Overview
Of hospitalised patients, 1 0- 15% develop hypophosphataemia, and a small proportion
have sufficiently profound depletion to lead to complications (e.g. rhabdomyolysis).
Causes
j1) Gastro-intestinal
a) Decreased dietary intake I Vomiting (prolonged, severe)
b) Decreased absorption (chronic diarrhoea, steatorrhoea, vitam in D
malabsorption)
c) Antacids (binding of ingested and secreted phosphate)
I 2) Renal losses
a) Hyperparathyroidism (HPT) (also associated with diminished
vitamin D)
b) Osmotic diuresis (salt, glucose)
c) Primary (isolated, Fanconi syndrome)
3) Redistribution (intracellular shift)

a) Re-feeding (stimulated by insulin)
b) Respiratory alkalosis, acute
c) 'Hungry-bone' syndrome
Key Objectives
• Appreciate that the likely causes are gastrointestinal, renal or redistributive.
• Select the most conservative form of therapy, since intravenous (IV)
phosphate salts are potentially hazardous.
Diagnose the cause of hypophosphataemia.
If no cause is clinically apparent, differentiate between redistribution,
gastrointestinal and renal causes by measuring fractional urinary
phosphate excretion.
62
• Conduct an effective plan of management for a hypophosphataemic
patient:
State that most patients will not require therapy other than repair of the
underlying causes.
Recognise that phosphate is a major intracellular anion and cellular
energy store component; and is a necessary additive in prolonged
parenteral nutritional therapy.
• Select patients with vitamin D deficiency for replacement with vitamin D.
83
005 Abnormal Serum Hydrogen lon Concentration
Overview
The hydrogen ion content of arterial blood is normally kept blandly alkaline at about
40 nanomolar ([H•] between 36 and 44 nmoi/L, which coincidentally equals a range of
pH from 7.44 to 7.36), by combined renal and respiratory regulatory mechanisms
together with extracellular and intracellular buffer systems.
Major adverse consequences may occur with severe acidaemia and alkalaemia despite
absence of specific symptoms (the range of extracellular hydrogen ion content
compatible with life is approximately 20-200 nmoi/L. This 10-fold change is expressed
in the pH notation as a change of one pH unit, e.g. from 7.8 to 6.8). The reversible
reaction H• + HC03- ...='" H 2 C0 3~ H20 + C02 forms the basis of renal and respiratory
control. The diagnosis of acid-base disorders depends on recognition of the clinical
setting and appropriate laboratory studies. It is crucial to distinguish acidaemia and
alkalaemia due to metabolic causes from those due to respiratory (gaseous) causes;
especially important is detecting the presence of both. Management of the underlying
causes and not simply of the change in hydrogen ion concentration is essential.
Causes
1) OOSA Metabolic acidosis
a) Addition of acid (high anion gap)

0 Endogenous acids (lactic acidosis, ketoacidosis, renal failure)
0 Exogenous acids (methanol, ethylene glycol, salicylate, etc.)
b) Loss of alkali/base (normal anion gap)
.J Gastrointestinal bicarbonate loss (e.g. diarrhoea, small bowel or
pancreatic fistula)
0 Renal bicarbonate loss (e.g. renal tubular acidosis, interstitial nephritis)
Serum I Plasma
Sodium 138 mmoi/L
Potassium 5.5 mmoi/L
Chloride 11 3 mmoi/L
Bicarbonate .(!. 15 mmoi/L
Urea 'G' 11 .5 mmoi/L
Creatinine 'G' 140 ,umoi/L
Lactate 0 3.2 mmoi/L
Arterial pH .a.7.28
P8 C02 30 mm Hg
Pa0 2 .Q. 70mm Hg
Mesenteric ischaemia and serum chemistry- metabolic (lactic) acidosis
64
j2) 0058 Metabolic alkalosis
a) Addition of alkali/base
U Milk-alkali syndrome
b) Loss of acid
0 Gastrointestinal loss of acid (gastric loss in vomiti ng, pyloric stenosis)
U Renal loss of acid (e.g. diuretics)
0 Associated with potassium loss (e.g. Conn syndrome - primary
aldosteronism)
Serum I Plasma
Sodium .0. 129 mmoi/L
Potassium .0. 2.9 mmoi/L
Chloride .0. 85 mmoi/L
Bicarbonate ~ 39mmoi/L
Creatinine 120 ,u moi/L
Arterial pH ~ 7.49
P3 C02 41 mm Hg
Pa0 2 100mm Hg
Pyloric stenosis and serum chemistry - hypochloraemic hypokalaemic

metabolic alkalosis
3) 005C Respiratory (gaseous) acidosis (due to decreased alveolar

ventilation, usually with attendant hypoxia)
a) Pulmonary causes of underventilation (e.g. chronic obstructive
pulmonary disease (COPD), upper airway obstruction, atelectasis
and sputum retention, pneumonia, interstitial lung disease,
pulmonary fibrosis, etc.)
b) Neuromuscular causes (e.g. wound pain, drugs, cerebral trauma and
coma, encephalitis, bulbar palsy, myasthenia, muscle paralysis)
4) 005D Respiratory alkalosis (due to increased alveolar

ventilation from overbreathing)
a) Psychogenic overbreathing from anxiety state
b) Miscellaneous (e.g. fever, drugs, salicylate, central nervous system
(CNS) disorders)
I 5) 005E Mixed acid-base disorders
85
Key Objectives
• In relevant clin1ca l situations. determine the possi bility of an acid-base
d1sorder by exammmg laborato ry pa rameters of: [H ]. P,.CO . [HCO ]. and
an1on gap.
• D1ag nose and treat the causal condition in conjunction with appropriate
additional measures to correct the abnormality and restore or mamtain
renal and respiratory funct ions.
• Through effic1ent. focused data gatherin g:
Diagnose the precipitatin g cause of acidaemia/alkalaemia exped itiously.
• Interpret crit1cai cli nical and laboratory findings which were key in the
processes of exclusion. differentiati on and diagnosis:
Select and Interpret appropnate investigations for various patients with
acidaemia/alkalaemia in order to identify the primary abnormality and
the adequacy of ti1e associated secondary ·compensation· (e. g. renal
failure with acidotic breathin g. pyloric stenosis with secondary renal
effects. etc.).
• Conduct an effective plan of management for a patient with acidaemia/
alkalaemia:
Outline general supportive measures.
Outline specific management for patients in each of the main groups.
Select patients who need speciali sed care and/or consultation.
66
006 Abnormal Serum Lipids
Overview
Abnormalities of serum lipid levels in Australian society due to dietary and other lifestyle
factors are very common. Secondary causes are relatively uncommon. Abnormal lipid
levels comprise one of the risk factors for arterial disease, particularly coronary artery
disease (CAD).
Identification is by screening of well adults, those with other risk factors and patients
with suspected or established CAD. Interpretation of results and their classification is
complex depending on the lipid profile found and the presence of other risk factors.
Levels can be modified by lifestyle changes and drug therapy, although the use of lipid
lowering agents to reduce risk is expensive.
Causes
1) Hypercholesterolaemia (elevated low-density
lipoprotein (LDL))
a) Primary causes
0 Polygenic (most common)
0 Familial hypercholesterolaemia (rare)
b) Secondary causes
0 Hypothyroidism
0 Obstructive liver disease
0 Nephrotic syndrome
0 Drugs (such as cyclosporine, thiazides)
I 2) Hypertriglyceridaemia
a) Primary causes
0 Dietary
0 Familial hypertriglyceridaemia
b) Secondary causes
0 Obesity
0 Diabetes mellitus
0 Chronic renal failure
0 Moderate ethanol use
I 3) Low high-density lipoprotein (HDL)

a) Obesity
b) Cigarette smoking
c) Inactivity
67
Key Objectives
• Identify persons at risk of CAD who would benefit from serum lipid
reduction .
• Conduct an effective management plan for a patient with abnormal serum
lipids, which includes behavioural change and possible drug therapy,
according to their overall risk of CAD.
• Understand the principles of population screening.
• Identify patients with secondary causes of lipid abnormalities.
• Interpret and integrate lipid profile with other risk factors for CAD.
• Specify lipid levels (especially LDL cholesterol) to be attained by treatment,
including a long term followup plan.
• Be aware of the range of therapeutic agents which lower serum lipids, their
indications, costs and side-effects.
68
007 Abnormal Liver Function Tests
Overview
Thorough investigation can distinguish benign reversible liver disease requiring no
treatment from potentially life-threatening conditions requiring immediate therapy. Drugs,
alcohol and infection (hepatitis) are the commonest causes. Liver function tests may
also assist in making the decision on whether some form of intervention is required .
Causes
1) Isolated hyperbilirubinaemia
a) Unconjugated or indirect
0 Haemolysis and ineffective erythropoiesis
0 Defects in transport into the hepacytes or intracellular conjugation:
• Gilbert disease
• Neonates
• Crigler-Najjar syndrome
b) Conjugated or direct- defect in transport out of the hepatocyte
0 Rotor syndrome, Dubin-Johnson syndrome
2) Hepatocellular (may lead to cirrhosis)

a) Alcohol , drugs, toxins (paracetamol, isoniazid)
b) Fatty liver and steatohepatitis
c) Viral hepatitis
d) Metabolic liver disease (haemochromatosis, Wilson disease, etc.)
e) Autoimmune chronic hepatitis
f) Shock or ischaemia
g) Septicaemia
I 3) Cholestatic
a) Intrahepatic
0 Drugs (oral contraceptives)
0 Infiltrative (amyloid, malignant)
0 Congestive (e.g. heart failure)
0 Autoimmune (primary biliary cirrhosis, sclerosing cholangitis)
0 Granulomatous disease
b) Extrahepatic (cholestasis from stone or neoplasm, stricture, atresia)
69
Hepatic metastases
Key Objectives
• Discuss abnormal laboratory tests in the context of the clinical presentation,
and select patients requiring medical or interventional management.
• Understand the effects of various toxins (e.g. drugs, alcohol, sepsis) on the
liver.
• Understand the liver's role in storage, synthesis and metabolism.
Differentiate between the causal conditions for abnormal liver function
tests.
Identify complications related to the presence of liver disease.
Select diagnostic tests appropriate for the identification of acute and
chronic liver diseases.
List the indications for abdominal ultrasound and ascitic fluid analysis.
List indications for liver biopsy.
• Conduct an effective plan of management for a patient with abnormal liver
function tests:
Select patients in need of hospitalisation.
List indications for active and passive prophylaxis against infective
hepatitis.
Counsel and educate patients about primary and secondary prevention
strategies for viral hepatitis (include public health measures).
Understand the role of monitoring liver function in terms of management
of a patient's illness.
70
008 Abnormal Serum Potassium Concentration I
Magnesium
OOBA Hypokalaemia
Overview
Potassium is the major intracellular cation. Of a total body potassium of 3,000 mmol in
adults, only two percent is in extracellular fluid (60 mmol) at a concentration of around
5 mmoi/L. Normal daily intake is also about 60 mmol ·Most excretion is in the urine
which is the source of most depletions, but abnormal gastrointestinal losses are also
important. Hypokalaemia usually indicates potassium depletion; and is most often
discovered on routine analysis of serum electrolytes or electrocardiogram (EGG) results.
Symptoms usually develop much later when depletion is quite severe (muscle weakness,
paralytic ileus, cardiac arrhythmias and sensitivity to digitalis). Hypokalaemia implies
a serum level below 3.5 mm oi/L. Potassium deficiency, metabolic alkalosis.
hypocalcaemia and hypomagnesaemia are commonly associated.
Causes
1) lncreasedlosses
a) Renal losses
0 Diuretics
0 Endocrine effects
• Prolonged steroid therapy
• Primary hyperaldosteronism (Conn syndrome)
• Secondary hyperaldosteronism (e.g. renovascular disease)
• Adrenal hyperplasia
• Cushing syndrome
• Ectopic adrenocorticotrophic hormone (ACTH)
b) Gastrointestinal losses
0 Vomiting - vomiting and pyloric stenosis; secondary renal losses occur
as well.
0 Bowel obstructions and prolonged gastrointestinal aspirates
0 Diarrhoea (villous adenoma of colorectum, laxative abuse,
inflammatory bowel disease (lBO), enteric fistula)
2) Decreased intake (e.g. anorexia nervosa, malnutrition)
3) Redistribution (familial periodic paralysis)
71
Key Objective
• Assess intake and shift of potassium into cells, select renal loss as the
category into which most problems fall, but remember gastrointestinal
causes of loss.
Differentiate between renal and gastrointestinal losses as causative
lesions.
Outline how urinary electrolytes assist in the elucidation of excess
losses of potassium.
• Conduct an effective plan of management for a hypokalaemic patient based
on sound principles:
Outline indications and guidelines for intravenous (IV) potassium
therapy.
72
Magnesium
0088 Hyperkalaemia
Overview
Hyperkalaemia (serum [K ·] greater than 5.5 mmoi/L) may produce serious side-effects
and may also be indicative of the presence of serious associated medical conditions.
Dangerous hyperkalaemia (greater than 6 mmoi/L) is rare if renal function is normal
despite significant release ot intracellular potassium into the extracellular phase in
response to the stress of injury, acidosis. sepsis and any catabolic state. Hyperkalaemia
is seen when renal failure and shock interfere with renal handling of potassium.
Causes
1) Reduced urinary excretion in renal failure and shock
a) Decreased glomerular filtration rate (GFR) in shock, acute or chronic
renal failure
b) Decreased tubular secretion in adrenal insufficiency
c) Effects of drugs on tubular function (angiotensin-converting enzyme
(ACE) inhibitors, nonsteroidal anti-inflammatory drugs (NSAIDs))
I 2) Redistribution
a) Red cell lysis
.J Rhabdomyolysis
.J Crush syndrome I Burns
.J Intravascular haemolysis
0 Tumour breakdown
b) Metabolic acidosis with normal anion gap
73
Key Objectives
• Diagnose true dangerous hyperkalaemia (greater than 6.0 mmoi/L), a
potentially lethal condition for which emergency treatment is the first
consideration , from pseudohyperkalaemia, due to cell lysis during
collection, and screen for causal conditions.
• Recognise that dangerous effects are confined to the heart, and cause
changes as in the electrocardiogram (ECG), arrhythmias and death.
• Recognise principles of emergency (temporary plus definitive) treatment of
dangerous hyperkalaemia.
Distinguish between life-threatening hyperkalaemia and
pseudohyperkalaemia utilising ECG.
Recognise signs of dangerous hyperkalaemia on ECG.
Distinguish between causes of hyperkalaemia by ruling out
redistribution or intake problems quickly, and concentrating on the more
common renal causes.
Identify patients with renal failure.
• Outline an effective emergency treatment plan for a dangerously
hyperkalaemic patient:
Select patients in need of specialised care and dialysis.
Understand principles of haemodialysis and peritoneal dialysis.
74
Magnesium
OOBC Hypomagnesaemia
Overview
Although hypomagnesaemia occurs in only about 10% of hospitalised patients, the
incidence rises to over 60% in severely ill patients. Hypomagnesaemia may be
responsible for otherwise puzzling clinical features in patients with prolonged illness.
Clinical features are mainly neuromuscular. Magnesium , like potassium, is a
predominantly intracellular cation and is poorly absorbed orally, so replenishment is
best by intravenous {IV) supplementation.
Causes
1) Gastrointestinal
a) Marked decrease in dietary intake
b) Diarrhoea, acute/chronic ; malabsorption and steatorrhoea, short gut
c) Acute pancreatitis
I 2) Renal loss
a) Diuretics (loop, thiazide, hypercalcaemia)
b) Volume expansion
c) Tubular dysfunction (alcoholics, aminoglycosides, amphotericin,
cisplatin , cyclosporin, acute tubular necrosis (ATN) in diuretic phase,
primary)
Key Objectives
• Determine which patients are likely to be hypomagnesaemic since
magnesium levels are not measured routinely.
• Evaluate patients with ventricular arrhythmias for possible
hypomagnesaemia, especially during ischaemic events and if diuretics
were prescribed.
75
Diagnose the cause of hypomagnesaemia.
• Interpret the critical cl inical and laboratory findings which were key in the
If no cause is clinically apparent, differentiate between gastrointestinal
and renal causes by measuring urinary magnesium excretion.
• Conduct an effective plan of management for a hypomagnesaemic patient:
Recognise that cellular uptake of magnesium is slow, and repletion
requires sustained correction.
Select potassium-sparing diuretics as an adjunct to management in
patients with diuretic-induced hypomagnesaemia if diuretic therapy
can not be stopped.
76
009 Abnormal Serum Sodium Concentration
009A Hyponatraemia
Overview
Serum sodium levels comprise the major determinant of extracellular fluid osmolality
and are normally held constant within a range of 135-145 mmoi/L by regulatory
mechanisms acting via sensitive hypothalamic osmoreceptor feedback, utilising
stimulation of antidiuretic hormone (ADH) by increased osmolality or vice versa. Causes
of increased ADH secretion, apart from hypertonicity of body fluids, include volume
depletion, stress, drugs and inappropriate sources of ADH from cerebral injury, tumours
or burns. The syndrome of inappropriate ADH secretion (SIADH) is seen quite commonly
in the setting of chest infections and other lung conditions and is an idiosyncratic reaction
of a number of drugs, particularly th iazide diuretics.
Hyponatraemia implies only a fall in the concentration of serum sodium and may be
associated with water gain, sodium depletion or often both.
Hyponatraemia (serum (Na+] less than 135 mmoi/L) is often detected in asymptomatic
patients because serum electrolytes are measured almost routinely. Minor abnormalities
often are transient and need no treatment. In adults or children with hyponatraemia,
the cause is usually iatrogenic, and the hyponatraemia dilutional rather than depletional.
Normally any fall in body fluid osmolality due to water overload is countered by the
excretion of excess water by the kidneys . Poor renal function with poor concentrating
power diminishes the ability to cope with excess water, which is also a feature of the
early period after major surgery.
Causes
11) Hypo-osmolar hyponatraemia
a) Water gain
0 Iatrogenic excess water administration (particularly after operations
and in children)
0 SIADH with decreased water excretion
b) Sodium depletion
0 Renal or extrarenal sodium and water loss with water replacement
in excess of electrolytes (enteric losses and fistulae , renal losses)
0 Addison disease
c) Oedema states
2) Non-hypo-osmolar hyponatraemia - associated with

hyperglycaemia or azotaemia
77
Key Objectives
• Recognition that hyponatraemia may mean water gain, sodium depletion or
a mixture of both.
• Recognition that minor abnormalities are often transient and need no
treatment.
• Identification of the main process is important because this will affect need
for and choice of therapy, and rate of correction.
• Recognition that water retention is spread over the whole body, and marked
intracellular oedema has its most severe effects on essential functions
causing mental confusion and ultimately coma.
Determine whether an increase in water relative to sodium exists
thereby expanding volume of cells or the change in sodium
concentration is artefactual or caused by hyperglycaemia.
Differentiate between sodium depletion and water gain by assessment
of volume status and/or the presence of an oedema state.
• Interpret critical clinical and laboratory findings which were key in the
processes of exclusion, differentiation, and diagnosis:
Interpret urinary electrolyte concentrations.
Interpret plasma and urinary osmolality.
• Conduct an effective plan of management for a patient with hyponatraemia:
Outline a therapeutic approach based on the underlying process.
Select the patients with hyponatraemia in need of specialised care or
consultation.
N.B. When serum sodium concentration is measured by flame photometry

or other methods requiring major dilution of plasma, hyperlipidaemia
or hyperproteinaemia may cause pseudohyponatraemia (iso-osmotic).
If sodium concentration is measured with a sodium selective
electrode on undiluted plasma (most laboratories today), a true
sodium concentration is obtained, and this type of
'pseudohyponatraemia' no longer exists.
78
009 Abnormal Serum Sodium Concentration
0098 Hypernatraemia
Overview
Hypernatraemia is often iatrogenic with solute administration in excess of the water
required to excrete it. Thirst is a sigmficant warning sign of hyperosmolar states in the
conscious patient. Hyp~rnatraemia is usually associated with inability to respond to
thirst by drinking water. Hypernatraemia is thus most likely to be encountered at the
extremes of life in the very young and in the very old, in comatose patients and in those
depending on tube or parenteral intravenous (IV) feeding .
Causes
1) Sodium gain (relative solute excess)
a) Excessively concentrated enteric or IV feeding solutions
b) Primary hyperaldosteronism (Conn syndrome)
2) Water depletion (true dehydration)

a) Water intake insufficient, inability of unconscious or incapacitated
patient to respond to thirst
b) Excess renal water loss - osmotic diuresis, diabetes insipidus
c) Excess insensible water loss- fever, overbreathing, burns
Key Objectives
• Recognition that hypernatraemia is almost always caused by a combination
of water loss with diminished ability to respond to thirst.
• Recognition of importance of careful monitoring of use of parenteral or
enteral feeding solutions in incapacitated patients to avoid hyperosmolar
hyperglycaemic hypernatraemic coma.
• Recognise that correction of the hypernatraemic state requires restoring the
water deficit to relieve and to reverse the hyperosmolar state, and restoring
normal urine output instead of continuing osmotic solute diuresis.
Determine the underlying cause of water loss and/or diminished thirst.
Determine the severity of the problem by assessment of patient's
volume status.
79
Evaluate urinary osmolality results in order to differentiate between
causes of water loss.
• Conduct an effective plan of management for a patient with
hypernatraemia:
Outline a therapeutic approach based on the underlying process.
Discuss potential side-effects of rapid replacement of water losses.
Select the patients with hypernatraemia in need of specialised care or
consultation.
80
010 Abnormalities of White Blood Cells
Overview
Because abnormalities of white blood cells occur commonly in both asymptomatic as
well as acutely ill patients. every clinician will need to evaluate patients for this common
problem. Most important to understand are the causes and clinical implications of
neutropenia and neutrophilia.
Causes
1) Leucopenia
a) Neutropenia
0 Decreased marrow production
• Drug-induced (alkylating agents, antimetabolites, antibiotics
(sulphonamides, penicillins, cephalosporins), anti-thyroid drugs
(carbimazole, propylthiouracil), anticonvulsant drugs (phenytoin,
carbamazapine , sodium valproate), anti-inflammatory drugs
(phenylbutazone, gold, diflunisal, penicillamine, naproxen),
antidepressants (amitriptyline, dothiepin, mianserin), antimalarial
drugs (maloprim, fansidar, chloroquine))
• Nutritional deficiency (vitamin B12 , folate)
• Sepsis
Viral (hepatitis, human immunodeficiency virus (HIV), influenza)
Bacterial (typhoid, tuberculosis (TB))
• Hypersplenism
Immune: rheumatoid arthritis (Felty syndrome); systemic lupus
erythematosus (SLE)
Nonimmune: severe portal hypertension
• Marrow infiltration
Malignancy: haematologic (acute and chronic leukaemia); non-
haematologic (carcinoma lung)
• Cyclic neutropenia
b) Lyphocytopenia
Drug-induced (glucocorticoids, cytotoxics)
0 Infections (HIV, TB)
0 Tumour-associated (lymphoma)
0 Acute illness (sepsis, myocardial infarction (MI))
0 Chronic illness (uraemia, congestive cardiac failure (CCF). SLE)
Marrow infiltration (vide supra)
81
c) Combined neutropenia and lyphocytopenia
0 Marrow infiltration (vide supra)
0 Drug-induced (cytotoxics)
0 Aplastic marrow (idiopathic, benzene, irradiation)
[ 2) Leucocytosis
a) Neutrophilia
0 Inflammation
• Infective - bacterial
• Noninfective
Tissue necrosis / Infarction I Trauma of burns
Autoimmune disorders: SLE/vasculitis
Gout
0 Neoplasia
• Myeloproliferative neoplasms, other malignancies
0 Drugs (glucocorticoids, lithium)
0 Acute stress or haemorrhage
0 Post-splenectomy
0 Leukaemoid reactions (white cell count (WCC) greater than
50.0 x 10 9/L - normal range 4.0 - 11 .0 x 109/L)
• Severe sepsis
Acute (septicaemia)
Chronic (TB)
• Malignancy
• Severe haemolysis
• {Chronic myeloid leukaemia is a myeloproliferative disorder not a
leukaemoid reaction)
b) Lymphocytosis
0 Infections (viral, TB, pertussis, other)
0 Acute and chronic lymphocytic leukaemia
0 Other (adrenal insufficiency)
Key Objective
• Interpret the clinical setting in which the leucocyte abnormality occurs as
this will often suggest the correct diagnosis and direct further investigation.
82
Distinguish between chronic conditions requiring non-urgent evaluation
and acute life-threatening illnesses requiring admission to hospital.
• Interpret critical clinical and laboratory findings important in formulating a
differential diagnosis:
Interpret the differential leucocyte count.
List the indications for bone marrow aspiration and biopsy.
• Conduct an effective plan of management for a patient with white blood cell
abnormalities:
Diagnose or exclude infection first as the cause of the leucocyte
abnormality.
Select patients for specialised care, including those with a neutrophil
cou nt of less than 1.0 x 109/L.
Counsel and educate patients with chronic leucocyte abnormalities.
83
011 Acutely Ill Infant/Child
011 A Paediatric Emergencies
Overview
Although paediatric emergencies such as the ones listed below are discu ssed with the
appropriate condition. the care of the patient in the paediatric age group demands
special skills.
Causes
1) Respiratory emergencies
(see #126 Wheezing/ Respiratory Difficulty/Stridor)
a) Upper respi ratory tract disorders (see #126A Upper Respiratory Tract
Disorders)
b) Lower respiratory tract disorders (see #1268 Lower Respiratory Tract
Disorders)
I 2) Infectious emergencies
(see #040 Fever and Chill s (Adult and Paediatric) and #1 028 Childhood
Communicable Disease With or Without Skin Rash)
I3) Cardiovascular emergencies

a) Arrhythmias (see #072 Palpitations (Abnormal Electrocardiogram
(ECG) I Arrhythmia))
b) Congestive heart failure (see #032A With Diffuse Chest X-Ray
Abnormality)
14) Fluid and electrolyte emergencies I

a) Dehydration I Volume depletion (see #098 Shock/Hypotension and
#0098 Hypernatraemia)
b) Hyperkalaemia (see #0088 Hyperkalaemia)
Is) Neurological emergencies

a) Seizures (see #095 Seizures (Epilepsy))
b) Febrile seizure
I 6) Abdominal emergencies
a) Abdominal pain (see #003E Anal Pain)
b) Abdominal distension (see #001 Abdominal Distension/Ileus)
84
17) Trauma
(see #018 Burns and #113 Trauma/Accidents/Prevention)
fa) Poisoning
(see #079 Poisoning)
9) Environmental emergencies (hypothermia I heat stroke)

(see #0400 Hypothermia and #040E Hyperthermia)
Key Objectives
• Recognise and manage effectively infants and children with life-threatening
paediatric emergencies.
• Describe the differences between paediatric and adult medicine and their
effect on emergency management.
Elicit symptoms and signs in a focused fashion for the assessment of an
infant/child in an urgent/emergent situation.
Perform physical examination and blood pressure (BP) measurement
and determine whether the patient is in shock.
• Conduct an effective plan of management for an infant/child in an urgent/
emergent situation:
Recognise special features of paediatric airway management.
List sites for intravenous (IV) access in the paediatric population.
Select patients in need of referral to intensive care units.
Outline initial management in a paediatric patient with seizures
including febrile seizures.
Outline initial management in a paediatric patient with acute sepsis.
85
011 B Crying/Fussing Child
Overview
A young infant whose only symptom is crying/fussing, challenges the doctor to distinguish
between the various causes, some of which can be serious.
Causes
11) Infections (systemic/focal)
2) Gastrointestinal/Intra-abdominal conditions
a) Infection
b) Inflammation
c) Intussusception
d) Constipation/Anal fissure
e) Diarrhoea
3) Trauma (neglect I child abuse I fracture)
4) Psychologic I Functional/ Hunger I Discomfort I

Boredom I Irritability
Key Objective
• Differentiate paediatric emergencies. including intussusception. from
conditions not requiring emergency treatment.
• Through efficient. focused data gathering:
Elicit a history of patient's previous behaviour, oral intake of food and
drink. vomiting , diarrhoea or constipation. and any medications
received.
Assess the parent-child emotional interaction.
86
Perform a full physical examination in order to identify the cause of the
illness with a focus on searching for sites of infection , intra-abdominal
conditions, increased intracranial pressure, cardiac and respiratory
disorders.
Differentiate serious from benign causes, and determine if a life-
threatening situation exists.
• Interpret critical clinical and laboratory findings which are key in the
Select investigations (when appropriate) to differentiate between acute
and benign disease.
• Conduct an effective plan of management for a crying/fussing child:
Counsel caregivers of crying/fussing children without organic disease.
Select chi ldren who require followup for additional investigation and
management.
Select patients in need of referral.
87
011 C Hypotonia I Floppy Infant
Overview
Children with decreased resistance to passive movement differ from those with
weakness and hyporeflexia. They requ ire detailed, careful neurologic evaluation.
Management programmes, often life-long , are multidisciplinary and involve patients,
family and community.
Causes
1) Central causes
a) ' Benign c ongenital hypotonia'
b) Cerebral malformations (holoprosencephaly); neurodegenerative
(leucodystrophy)
c) Seizures, trauma (subarachnoid or subdural haemorrhage)
d) Hydrocephalus / Increased intracranial pressure
e) Infectious causes (e.g. encephalitis, abscess, meningitis)
f) Neoplasms
g) Hypoxic/lschaemic encephalopathy
h) Effects of toxins and drugs
I 2) Neural disease, peripheral

a) Anterior horn cell (e.g. progressive spinal muscular atrophy, spinal
cord infarction)
b) Peripheral nerves I Polyneuropathies (trauma)
c) Myoneural junction (myasthenia gravis, botulism)
I 3) Muscular disease
a) Muscular dystrophy
b) Myotonic dystrophy
c) Congenital myopathies
d) Inflammatory myopathies (dermatomyositis I polymyositis)
4) Metabolic/Electrolyte causes (hypokalaemia, hypoglycaemia,

etc.)
5) Other genetic causes (trisomy 21, Prader-Willi syndrome,

Niemann.Pick disease, Tay..Sachs disease)
88
Key Objectives
• Determine the presence of conditions amenable to rapid treatment
(electrolyte imbalance, seizure, infection , intracranial bleeding,
hydrocephalus).
• Differentiate infants with generalised hypotonia from those with weakness
and hyporeflexia.
Determine birth history, age and rapidity of onset and progression of
symptoms.
Determine whether lesion is localised or general, through appropriate
observation of posture, together with neurological, muscle and joint
examination .
• Interpret critical clin ical and laboratory findings which were key in the
processes of exclusion. differentiation and diagnosis:
Select investigations to differentiate central from neuromuscu lar causes
(e.g. computed tomography (CT) versus serum creatine kinase (CK).
electromyelography (EMG). muscle biopsy).
Determine which children requ ire genetic studies.
• Conduct an effective plan of management for a floppy infant:
Determine whether respiratory status is adequate or intubation is
required .
Counsel families with afflicted children about management, prognosis
and genetic implications.
Develop a management plan that involves the family and community
resources .
89
012 Anaemia and Pallor
Overview
Anaemia may be the sole manifestation of serious medical disease. Anaemia may be
due to blood loss, decreased production or increased destruction of red blood cells.
Simple tests may provide important information. Key to an understanding of anaemia
is a full blood examination (FBE) (which includes a blood film). This wi ll give an indication
as to both the aetiology and the severity of the anaemia, and will guide the direction for
further investigation.
Causes
1) Normocytic
a) Decreased production (bone marrow disease, reduced

erythropoietin, drugs)
b) Increased destruction
0 Red blood cell (RBC) abnormalities
0 Auto-antibodies
0 Drugs
c) Blood loss (visible, occult)
d) Apparent (dilutional anaemia, e.g. of pregnancy)
2) Mic roc yti c (iron d efi c i e n c y , c hronic blood lo ss,

h ae moglobinopathi es )
3) Macrocytic (folate, vitamin B 12 defic iency, chemotherapy,

alcohol abu s e)
Iron deficiency anaemia - carcinoma caecum
90
Key Objectives
• Be able to interpret a blood count and film.
• Understand that iron deficiency anaemia may indicate the presence of
serious gastrointestinal disease.
• By considering the clinical context, determine if anaemia is present, since
all three laboratory indices of anaemia are concentration measurements.
• Interpret the signs and symptoms of anaemia with the understanding that
they are dependent on the rapidity with which anaemia developed.
Determine the presence of anaemia and differentiate between the
various causes, according to the patient's age.
Select a causal classification of anaemias using red cell morphology.
Outline diagnostic plans for an adult presenting with an iron-deficiency
anaemia.
• Conduct an effective plan of management for a patient with anaemia:
Outline treatment of iron deficiency anaemia.
Outline treatment of vitamin deficiency anaemias.
Select patients in need of referral for haematological consultation and
care (e.g. haemolysis, bone marrow disease).
Conduct counselling and education of patients with anaemia caused by
nutritional deficiencies and haemoglobinopathies.
91
013 Attention Deficit I Learning Disability
Overview
Doctors may be confronted by developmental and behavioural problems of childhood
and adolescence and required to liaise with other caregivers.
Causes
Learning disability - differential diagnosis includes:
1) Global cognitive problem (mental retardation or borderline IQ)
2) Sensory impairment (auditory/visual)
3) Family emotional disturbance: oppositional defiant I conduct

disorder
14) Anxiety/Mood disorders
5) Developmental coordination disorder
I6) Dyslexia
7) Attention deficit hyperactivity (hyperkinetic) disorder (ADHD)

a) Predominantly inattentive
b) Hyperactive/Impulsive
c) Combined
I8) Pervasive developmental disorder

a) Autistic disorder
b) Rett disorder/syndrome
c) Childhood disintegrative disorder
d) Asperger disorder
9) Communication and language
10) Child abuse or neglect
11) Chronic medical disease
12) Tic disorder
13) Drug or alcohol d e p endence
92
Key Objectives
• Make a clinical assessment of a child's developmental level.
• List the criteria of ADHD .
Determine whether environmental factors in school or family may be
contributing to school failure.
Determine whether there is a family history for attention deficit or any of
the comorbid conditions.
Determine whether there is evidence of developmental delay, genetic
syndromes, encephalopathies, or poisoning (e.g. alcohol, lead).
Select patients who require further investigation or psychological
testing.
• Conduct an effective plan of management for a patient with school failure:
Along with other caregivers , outline a management plan which includes
(when appropriate):
Parent, child and teacher education and other educational
interventions.
* Structured educational and recreational activities.
* Behavioural management strategies.
* Psychological counselling.
Medication.
Discuss the use of medication (amphetamine derivatives) in the
treatment of ADHD.
93
014 Behaviour Disorder
(See also #026 Development Disorder J Developmental Delay)
Overview
Clinicians are usually the initial caregivers to be confronted by the developmental and
behavioural problems of childhood and adolescence, wh ich can lead to impaired social,
academic and occupational functioning. The behaviour disorders are more common in
males, eating disorders are more common in females. The early diagnosis of autism is
particularly difficult.
Causes
1) Attention deficit hyperactivity (hyperkinetic) disorder (ADHD)
2) Oppositional defiant I Conduct disorder
3) Eating disorders (anorexia nervosa I bulimia, pica, rumination

disorder)
4) Sleep disorders (nightmares, sleep terror disorder,

sleepwalking, enuresis)
5) Tic disorders (Tourette syndrome, motor or vocal tic disorders)
js) Autism
Key Objective
• Determine whether the patient has a behaviour disorder or some other
underlying medical condition, mood disorder or a comorbid developmental
disability.
94
• Through efficient, focused data gathering, which includes assessment of
family history, context and culture:
Determine whether the patient requires consultation with a psychiatrist/
psychologist for oppositional defiant or conduct disorder.
Determine whether criteria for anorexia/bulimia are present (on history
and physical examination).
Determine whether a patient with a tic disorder requires referral to a
paediatrician, neurologist, or child psychologist.
Determine whether a patient with a sleep disorder requires further
investigation or specialist referral.
Select patients requiring further investigation.
• Conduct an effective plan of management for a patient with behaviour
disorder:
Discuss indications for hospital admission in a patient with an eating
disorder.
In a patient with an eating disorder, outline a management plan
including (when appropriate) psychotherapy (individual and family) ,
behaviour modification techniques, nutritional therapy, and medication.
95
015 Bleeding Tendency I Bruising
Overview
A bleeding tendency can manifest with cutaneous and/or systemic features. It may
signify a drug-induced disorder, a problem of haemostasis or a vessel abnormality.
Taki ng a detailed history (including a family history) is essential.
Causes
1) Platelet problem
a) Decreased number
0 Decreased production (e.g. leukaemia)
0 Increased destruction
0 Abnormal sequestration
b) Abnormal function
Congenital
0 Acquired
• Drugs (aspirin)
• Renal disease
I 2) Coagulation factor problem I

a) Congenital
0 Factor VIII deficiency
0 von Willebrand disease
0 Factor IX deficiency
b) Acquired
0 Liver disease
0 Anticoagu lants
0 Disseminated intravascular coagulation (DIC)
Vitamin K deficiency
0 Inhibitors
0 Drugs (heparin-induced thrombocytopenia)
0 Massive blood transfusion
13) Vessel problem

a) Congenital (collagen disorders)
b) Acquired (steroids, vasculitis)
96
Key Objectives
• Understand the role of a clinical history in determining the cause of a
bleeding disorder.
• Be aware of the appropriate clinical signs and tests that will help to
determine the underlying cause of a bleeding disorder.
Differentiate between platelet problems, coagulation factor problems,
and vessel problems.
Select investigative tests appropriate for platelet, coagulation, and
vessel problems.
Contrast the results and their interpretation.
Select 'at risk' families for investigation of potentially affected children.
• Conduct an effective plan of management for a patient with bleeding
tendency or bruising:
Select platelet transfusions, vitamin K, and plasma derivatives in the
management of patients with bleeding disorders according to the
diagnosis made.
Formulate a management plan for the reversal of the anticoagulant
effect of heparin, warfarin or aspirin.
Retroperitoneal haemorrhage following warfarin
97
016 Bleeding with Defaecation I Acute Lower
Gastrointestinal Bleeding I Melaena I Occult Blood
in Stool I Prevention of Cancer
Overview
Occult gastrointestinal bleeding may be due to serious gastrointestinal disease
(carcinoma of the colon or stomach). Screening the stool for occu lt blood in high-risk
groups may increase diagnostic yield.
Bright red blood unmixed with the stool noticed at the time of defaecation is usually due
to a benign anorectal cause , but other associated serious pathology must be excluded.
Acute lower gastrointestinal bleeding with fresh blood and clots independent of
defaecation is usually colonic and associated with colonic diverticula. Localisation of
the bleeding source can be difficult.
Melaena (a black tarry stool), with or without haematemesis, almost invariably signifies
significant upper gastrointestinal haemorrhage.
Causes
1) Upper gastrointestinal bleeding with melaena
(see #048 Haematemesis/Melaena)
I2) Lower gastrointestinal bleeding

a) Colorectal cancer/polyp
b) Anorectal disease (haemorrhoids, anal fissure, acute or chronic)
c) Colonic diverticulosis
d) Angiodysplasia
e) Enterocolitis (ischaemic, infectious, inflammatory bowel disease
(180), nonsteroidal anti-inflammatory drugs (NSAIDs))
f) Other (small bowel neoplasms, Meckel diverticulum)
Occult blood in stool
Carcinoma rectum Prolapsed haemorrhoids
98
Key Objective
• List the three key steps in the management of the separate presentations of
lower gastrointestinal bleeding as: resuscitation and assessment;
localisation; and diagnosis and treatment.
Define the relationship between bleeding and defaecation.
Undertake an appropriate examination to determine the cause of the
bleeding.
List and diagnose the most likely cause of blood in the stool.
Identify patients requiring urgent assessment and treatment.
List and diagnose the presence of associated medical cond itions
predisposing to the development of colorectal cancer.
• Interpret critical cl inical and laboratory find ings which were key in the
List advantages and disadvantages for anoscopy, rectoscopy,
sigmoidoscopy, colonoscopy versus barium studies, radionuclide
imaging, and angiography in patients with blood in the stool and the
appropriate time to perform these.
Select asymptomatic patients in need of screening for colorectal cancer.
Outline the diagnostic value and limitations of contrasting
haematochezia (fresh blood in stool) and melaena.
• Conduct an effective plan of management for a patient with blood in stool:
Select patients in need of immediate therapy.
Contrast diagnostic and management plans for patients with persisting
acute lower gastrointestinal haemorrhage with plans for evaluation of
intermittent passage of bright blood unmixed with the stool.
Evaluate patients in a cost-effective manner.
Outline the assets and limitations of screening using faecal occult blood
testing.
99
017 Breast Disorders
017A Male (Gynaecomastia}
Overview
Physiologic gynaecomastia is common in the newborn, in adolescence, and in males
over 50 years of age. In pathologic gynaecomastia, a definite aetiology is found in the
minority; but a careful drug history is important to detect a treatable cause , as is clinical
screening for occult malignancy. An underlying feature is increased oestrogen to
androgen ratio.
Causes
1) Physiologic gynaecomastia
a) Newborn
b) Adolescence
c) Ageing (SG-80 years; decreased testosterone or increased binding
globulin)
I2) Pathologic gynaecomastia I

a) Deficient production or action of testosterone
0 Anorchia
0 Defects in testosterone synthesis
0 Orchitis
0 Renal failure
b) Increased oestrogen production
0 Testicular tumours
0 Other tumours producing human chorionic gonadotropin (hCG)
0 Klinefelter syndrome
0 Hyperthyroidism
0 Liver disease
0 Obesity
0 Malnutrition/Starvation
c) Drugs
0 Oestrogens/Oestrogen-like (oral contraceptive pill (OCP), digitalis)
0 Anabolic steroids in body-builders
0 Inhibitors of testosterone synthesis or action (spironolactone,
cimetidine, flutamide)
0 Other drugs (methyldopa, captopril, tricyclics)
d) Idiopathic
10 0
Key Objectives
• Differentiate between gynaecomastia and breast cancer.
• Differentiate between gynaecomastia and pseudogynaecomastia (fat
deposition without glandular proliferation).
Differentiate patients with gynaecomastia due to physiologic or
pathologic causes.
• Identify patients who require further investigation.
Select and interpret laboratory tests in the investigation of
gynaecomastia.
Select and interpret imaging tests and cytology/histology in the
investigation of gynaecomastia.
• Conduct an effective plan of management for a patient with gynaecomastia:
Diagnose patients with physiologic gynaecomastia who require no
specific therapy.
Diagnose patients with drug-induced gynaecomastia who would benefit
from withdrawal of the drug.
Identify patients requiring surgery.
Gynaecomastia
101
0178 Female (Breast Lump 1 Prevention of Cancer I

Screening}
Overview
Breast cancer is the most common cancer in women. One in 13 Australian women will
develop breast cancer in their lifetime. Screening women over 50 years and other
high-risk groups by regular two-yearly mammography improves survival and identifies
small preclinical lesions. A small but significant proportion of patients have fami lial
cancer in whom genetic screening and counselling may be helpful.
Causes
1) Breast carcinoma (the most important, aHhough
not the most common cause of a breast lump)
a) Non-invasive
0 Ductal carcinoma-in-situ (DCIS)
0 Lobular carcinoma-in-situ (LCIS)
b) Invasive
Invasive ductal carcinoma
0 Invasive lobular carcinoma
Others (tubular, medullary, papillary, mucinous)
2) Diffuse nodularity - fibrocystic change
3) Discrete benign breast lumps ('domi nant lumps')

a) Localised fibrocystic change
b) Gross cysts
c) Galactoceles
d) Fibroadenomas
e) Traumatic fat necrosis
f) Mammary duct ectasia
14) Breast infections

a) Associated with lactation - lactational mastitis I breast abscess
b) Not associated with lactation - mammary duct ectasia, subareolar
abscess, mamillary fistula
5) Rarer causes- phyllodes tumour (usually benign- and only

locally invasive, occasionally true sarcoma)
--------------~
102
Key Objectives
• Ability to perform a standardised clinical breast examination, ensuring
correct patient comfort and positioning, and appropriate technique.
• Ability to distinguish normal from abnormal and suspicious findings.
• Understanding risk factors for development of breast cancer in women.
• Understanding the investigations for mammography and breast ultrasound
and the appropriateness of each for different clinical situations and age
groups.
• Understanding the principles of management of breast cancer by surgery
and adjuvant means.
Determine which women are at high risk for breast cancer.
• Interpret critical clinical and laboratory findings , which were key in the
• Identify groups based on age or other pre-existing risk factors for regular
screening mammography; outline benefits and drawbacks of screening
programmes.
• Identify families in whom genetic screening and counselling may be
considered; outline the benefits and drawbacks of genetic screening.
• Counsel and educate patients on the role of breast self-examination.
• Conduct an effective diagnostic/management plan for a patient presenting
with a breast lump:
Outline an algorithm for diagnosis of a patient presenting with a breast
lump. Which patients do NOT require surgery?
Outline the indications for percutaneous fine needle aspiration cytology
(FNAC) and core biopsy in patients with breast pathology.
Outline the indications for surgery, radiotherapy, hormonal antihormonal
therapy, and chemotherapy in women with breast cancer.
Outline the indications for breast-conserving surgery in women with
breast carcinoma.
Counsel women with risk factors for the development of breast cancer
on the utility of screening.
103
L
. .
4(.~
Breast cyst - mammogram and ultrasound
Screen-detected cancer
Screening mammogram
excision
Mammogram -carcinoma of breast
104
017C Nipple Discharge 1 Galactorrhoea
Overview
Nipple discharge is a ~ommon symptom of concern to the patient. Spontaneous
discharges are of more significance than those evoked only by squeezing, as are bloody
discharges from a single duct. In the absence of an accompanying lump, the cause is
almost always benign. Although milky breast secretions may be noticeable (and are
normal) in 25% of previously pregnant women , spontaneous persistent galactorrhoea
may reflect underlying breast or endocrine disease and requires investigation.
Causes
1) Nipple discharge
a) Bloody: breast neoplasm, usually benign duct papilloma
b) Serous, green, yellow-brown: usually benign fibrocystic change
c) Toothpaste, worms: mammary duct ectasia
2) True galactorrhoea (fat droplets present)

a) Autonomous prolactin production
0 Pituitary tumours (micro- or macro-adenoma)
Ectopic production of prolactin (bronchogenic or renal cell cancer)
b) Enhanced prolactin release
Hypothyroidism
0 Sucking reflex
c) Failure to inhibit release of prolactin
0 Pituitary stalk section or compression by mass lesion
0 Drugs (phenothiazines, methyldopa, opiates)
d) Idiopathic (most common cause)
Key Objectives
• Identify patients with nipple discharge requiring surgery.
• Differentiate between nipple discharge and galactorrhoea.
• Differentiate physiological from pathological galactorrhoea.
105
Identify patients with spontaneous or evoked, unilateral or bilateral,
single or multiple duct discharges and different types of discharge.
For galactorrhoea, determine which patients have menstrual
irregularities or visual field defects since they are likely to have an
underlying disease.
Select and interpret laboratory tests and diagnostic imaging in patients
with nipple discharge/galactorrhoea.
• Outline an effective plan of diagnosis and management for a patient with
nipple discharge:
Determine which patients are likely to have a breast neoplasm.
Outline the role of surgery in patients with nipple discharge
List the medications which can cause galactorrhoea.
Outline the role of bromocriptine and other dopamine agonists in the
management of patients with hyperprolactinaemia and galactorrhoea.
Counsel and educate patients with chronic galactorrhoea how the
galactorrhoea may be minimised.
106
017D Breast Pain (Mastalgia}
Overview
Breast pain is a very common symptom in women. It is rarely caused by malignant
disease, and pain severity varies widely. Mastalgia is most common between the ages
of 3D-50 years ; it is unusual after the menopause, apart from those patients on hormone
replacement therapy (HRT). Pain may be cyclical or non-cyclical, bilateral or unilateral.
Pain is a feature of acute infections (mastitis I breast abscess) complicating lactation.
Causes
1) Cyclical mastalgia and nodularity (two-thirds)
12) Non-cyclical mastalgia
13) Focal mastitis/abscess
4) E.xtramammary causes (costochondritis I Tietze syndrome,

musculoligamentous strain, etc.)
Left breast abscess
Key Objectives
• Exclude focal treatable lesions (inflammations, infections, neoplasms).
• Arrange treatment according to severity and with appropriate reassurance
as to benign aetiology.
Identify focal or diffuse infective mastitis and treat appropriately with
antibiotics, expression or drainage.
process of exclusion, differentiation and diagnosis.
Select appropriate investigations in a patient with mastalgia.
• Conduct an appropriate step-wise plan of management for a patient with
mastalgia.
107
017E Breast - Skin Changes
Overview
Skin changes involving the breast, nipple and areola may indicate tethering or invasion
from an underlying carcinoma. Physical examination should be meticulous to identify
suspicious features.
Causes
1) Nipple and areola
a) Paget disease - underlying duct carcinoma
b) Simple dermatitis/eczema
c) Benign squamous papilloma of nipple, accessory nipple(s)
d) Enlarged/Inflamed sudoriferous gland (Montgomery follicle)
e) Retraction- significant if recent and fixed (underlying carcinoma)
I 2) Skin of breast
a) Skin dimple and tethering over carcinoma (may only be evident on
raising arms)
b) ' Peau d'orange' - due to dermal oedema (neoplastic or inflammatory)
c) Subcutaneous 'string' from lymphangitis (Mondor disease)
d) Intertrigo (common beneath pendulous large breasts)
e) Mamillary sinus/fistula (secondary to mammary duct ectasia)
f) 'Pseudolipoma' - (prominence of compressed fat overlying a deeper
carcinoma)
Paget disease of nipple Accessol}' nipple
108
Cancerous skin dimpling Peau d'orange
Key Objectives
• Ability to identify skin, nipple and areola abnormalities on physical
examination.
• Ability to identify suspicious lesions requiring further investigation.
Identify abnormalities of skin and nipple requiring further assessment.
Outline appropriate diagnostic and management plans for a patient
presenting with nipple eczema.
Conduct appropriate management plans for a patient with a mamillary
fistula.
109
018 Burns
(See also # 113C Burn Injuries)
Overview
Burns range from minor cutaneous wounds to massive life-threatening traumas, and
remain a frequent cause of accidental death, and of gross burn morbidity. Many
domestic and industrial accidents are preventable. Public education concerning risks
and their avoidance is of major importance.
Causes
1) Scalds (hot water spills are commonly partial thickness, molten
metal spills cause full thickness localised burns)
2) Flame burns (commonly full thickness)
3) Burns from radiant heat and hot objects
4) Electrical burns (high amperage and voltage electrical burns

add risks of electrocution)
5) Chemical burns (cause additional damage by continuing

contact)
I6) Requiring special care

a) Partial thickness (second degree) and full thickness (third degree)
greater than 10% body surface area (BSA) in patients aged less than
10 and more than 50 years or greater than 20% any age
b) Second and third degree greater than 15% BSA require Intravenous
(IV) replacement; greater than 20% BSA require urinary catheter
c) Second and third degree on face, hands, feet, genitalia, perineum,
major joints
d) Third degree greater than 5% BSA
e) Electrical burns (Including lightning) and chemical burns
f) Circumferential burns
g) Burns plus other serious Illness
110
Key Objectives
• Perform assessment and initial treatment of burn patients according to
emergency management of severe trauma (EMST) protocol: primary
survey, secondary survey, etc.
• Diagnose burns according to:
Percentage BSA involved ('rule of nines', modified in children).
Depth of skin injury.
Partial th ickness burns (first and second degree) - erythema, blistering,
moist exudates, soft, painful to pinprick, circulation present.
Full thickness burns (third and fourth degree) - dull white, opaque,
brown and charred, visible thrombosed veins, dry, firm , painless to
pinprick, no capillary response .
• Outline effective management plans for:
The burned patient.
The burn wound.
Determine the BSA affected first, since depth is difficult to determine
initially.
After 24 hours, determine depth of skin injury (first degree to fourth
degree).
Determine whether there are other associated clinical problems or other
trauma.
Determine patient's tetanus immunisation status.
Determine whether inhalation injury has caused respiratory distress.
Superficial scald burns
111
Determine whether carbon monoxide poisoning has occurred by
measuring carboxyhaemoglobin.
• Conduct an effective plan of management for a patient with severe burns:
Outline initial management in a burn patient who will require referral
including stopping further burn injury, covering of burn area, and
resuscitation with oxygen, IV fluids, and physiologic monitoring.
Outline initial topical antibacterial treatment.
Discuss mechanism of injury of electrical burns and need for cardiac
and renal monitoring.
• Outline an appropriate initial plan of IV fluid replacement
(e.g. %BSA x kg weight x 2 ml fluid in first 24 hours- one-third first 4 hours,
one-third next 8 hours, one-third next 12 hours).
Full thickness bums - legs
Superficial bums - face
112
019 Cardiac Arrest I Respiratory Arrest
Overview
Most cases of cardiac arrest occur secondary to a cardiac arrhythmia. The ability to
perform and manage cardio-pulmonary resuscitation effectively is a pre-requisite for
all medical graduates.
Causes
1) Tachyarrhythmias (marked)
a) Ventricular fibrillation/tachycardia
b) Atrial fibrillation/flutter
I2) Bradyarrhythmias I Asystole

a) Sinus bradycardia I Arrest I Sick sinus syndrome
b) Third degree block (slow/absent escape rhythm)
I 3) Acute vascular occlusion

a) Myocardial infarction (MI)
b) Obstruction of cardiac filling
0 Pulmonary embolus (massive)
0 Acute cardiac tamponade
0 Tension pneumothorax
c) Mechanical heart valve blockage
I 4) Cardiac/Vascular ruptures
a) Type I dissecting aortic aneurysm
b) Ventricular rupture
c) Mitral papillary muscle rupture with torrential mitral regurgitation
I 5) Vasodepressor collapse
a) Neurocardiogenic collapse
b) Hypersensitive carotid sinus syndrome
c) Marked orthostatic hypotension
113
Key Objective
• Be confident and competent in your ability to manage a cardio-pulmonary
arrest.
• Conduct an effective plan of management for a patient with cardiac arrest I
respiratory arrest:
Evaluate the status of the airway and provide respiratory support as
indicated.
Demonstrate the techniques of cardiopulmonary resuscitation (CPR)
according to the age of the patient.
Identify and interpret quickly the signs of impending and actual cardiac
and/or respiratory arrest.
Differentiate between the possible causes of the cardiac and/or
respiratory arrest.
Select and interpret appropriate investigations for patients presenting
with cardiac and/or respiratory arrest, including electrocardiography,
chest X-ray, serum electrolytes, and blood gases.
If the resuscitation attempt was not successful, communicate, with
sensitivity, the news of death to family members and discuss the
possibility of an autopsy if indicated; if resuscitation is successful,
communicate with sensitivity, the news to the family and answer all
pertinent questions.
114
020 Chest Discomfort
Overview
Chest pain may be central or peripheral. Central chest pain is a common presentation
of cardiac disease, but it may also be due to disease of the lungs, gastrointestinal tract
or a musculoskeletal disorder. Coronary artery disease (CAD) is a potential life-
threatening disease. Doctors must recognise the manifestations of CAD and the key
characteristics that help to distinguish cardiac pain from other causes of chest pain.
Causes
11) lschaemic heart disease
a) Acute myocardial infarction (MI)
b) Angina pecto ris (stable, unstable, microvascular, coronary spasm)
12) Mitral valve prolapse
I 3) Aortic dissection
a) Hypertensive
b) Cystic medial necrosis, Marfan syndrome, Ehlers-Danlos syndrome
c) Connective tissue disease
d) Syphilis
14) Pericarditis
a) Infective
0 Viral (Bornholm disease)
0 Bacterial
b) Noninfective
0 Post-myocardial infarction
0 Post-coronary artery bypass graft (CABG)
0 Uraemic
0 Connective tissue disease
5) Pulmonary causes (embolism, pneumonia,

pleuritis, pneumothorax, etc.)
I 6) Chest wall origin

a) Costochondritis (Tietze syndrome)
b) Herpes zoster
115
I 7) Psychogenic
a) Anxiety, hyperventilation syndrome
b) Cardiac neurosis
8) Neoplasia (lung carcinoma, mediastinal malignancy)
Key Objectives
• Know the key characteristics that help to distinguish cardiac and non-
cardiac sources of chest pain.
• Differentiate between Ml and other forms of CAD early, in order to take
advantage of potential life-saving therapy.
Differentiate cardiac pain from other types of visceral pain.
Differentiate Ml from unstable and stable angina.
Select and interpret electrocardiograms (ECGs) and cardiac enzymes,
and discuss newer biochemical markers (such as troponin).
Select and interpret diagnostic imaging of the chest.
• Conduct an effective plan of management for a patient with chest pain:
Outline initial management of stable and unstable angina, acute Ml, and
other causes of chest discomfort.
List indications and contraindications of thrombolytic therapy and list
potential complications.
Select patients in need of specialised care and/or consu ltation.
Counsel patients with chest pain caused by life-threatening conditions
and counsel their families.
Identify the coronary risk factors and define a plan of management for
these where appropriate.
State the long term management of patients after Ml, including
secondary prevention strategies.
Select cost-effective investigative and therapeutic modalities .
Discuss primary and secondary preventive strategy education for
patients with ischaemic heart disease.
11 6
021 Coma I Impaired Consciousness
Overview
Patients with altered level of consciousness account for five percent of hospital
admissions. Causes range from those which are rapidly treatable and recoverable, to
those causing severe morbidity and mortality. Management of prolonged coma requires
expert and intensive nursing and medical care and monitoring for changing levels of
consciousness.
Causes
11) Metabolic encephalopathy
a) Drugs or toxins (e.g. alcohol)
b) Electrolyte abnormalities (hyponatraemia/hypernatraemia,
hypercalcaemia, hypoglycaemia)
c) Liver or renal failure
d) Hypertensive encephalopathy
e) Hypoxaemia/Hypercapnia
f) Sepsis (systemic)
I 2) Structural brain damage

a) Hemispheric (haemorrhage, ischaemia/infarction, neoplastic,
traumatic)
b) Brainstem (haemorrhage, ischaemia/infarction, neoplastic,
traumatic)
I 3) Infectious
a) Central nervous system (CNS) (meningitis, encephalitis)
b) Non-CNS (sepsis)
14) Miscellaneous
a) Seizure (post-ictus)
b) Myxoedema
I 5) Malingering
117
Key Objective
• Diagnosis and management of coma relies on the knowledge of the
potential causes, an interpretation of simple clinical signs and the efficient
use of diagnostic tests.
Determine the most likely cause for, and seriousness, of coma by
means of physical examination leading to rational investigation.
Conduct a clinical assessment of the level of consciousness .
Select and interpret laboratory investigations for patients suspected of
metabolic encephalopathy.
Select diagnostic imaging appropriate for comatose patient.
• Conduct an effective plan of management for a patient with coma/impaired
consciousness:
Define level of consciousness utilising the Glasgow Coma Scale.
Select patients in need of immediate therapy and perform initial
treatment.
Outline potential issues of importance in the ethical management of the
incompetent patient, including those of consent for treatment and
advanced directives.
Conduct assessment for suspected brain death prior to referring patient
to neurological specialist for the definitive diagnosis of brain death.
118
022 Confusion/Delirium I Acute Brain Syndrome
Overview
Delirium is a common and serious problem, particularly in the elderly, the hospitalised
and postoperative patients. It represents a disturbance of consciousness and cognitive
impairment with reduced ability to focus, sustain, or shift attention (The Diagnostic and
Statistical Manual 4 - Text Revision (DSM-IV-TA)). This disturbance tends to develop
over a short period of time (hours to days) and tends to fluctuate during the course of
the day. It is often associated with a disturbance of both the sleep-wake cycle and
psychomotor behaviour. It may be superimposed on a dementing process or it may
have multiple contributing factors . A clear understanding of the differential diagnosis
enables rapid and appropriate treatment.
Causes
j 1) Systemic
a) Intoxication/Withdrawal
0 Drugs (opiates, psychotropics, anticholinergics, corticosteroids,
cannabis, alcohol, amphetamines, hallucinogens)
0 Withdrawal (alcohol, opiates, psychotropics)
0 Poisoning I Toxins I Heavy metals
b) Metabolic
0 Hypoxaemia
0 Electrolyte disturbances (hyponatraemia/hypernatraemia,
hypercalcaemia)
0 Hypoglycaemia
0 Organ failure {uraemia, hepatic encephalopathy, hypoxaemia,
hypercarbia, heart failure)
0 Hypertensive encephalopathy
0 Hypoalbuminaemia
0 Porphyria
0 Thiamine deficiency
c) Miscellaneous
0 Systemic sepsis, pneumonia, urinary tract infections (UTis),
encephalitis, acquired immune deficiency syndrome (AIDS)
0 Postoperative states (residual anaesthetics, stress, sleep deprivation,
cataract surgery, fat embolism, anaemia)
0 Endocrinopathies (thyroid, adrenal)
0 Burns/Electrocution
0 Hyperthermia
119
2) Local (central nervous system (CNS))
a) CNS infections
b) Acute vascular events (stroke, migraine, vasculitis, carotid stenosis)
c) Neoplasm and paraneoplastic processes
d) Epilepsy
e) Post~lectroconvulsive therapy
f) Post-head injury
Key Objective
• Differentiate delirium due to general medical conditions from dementia,
drug intoxication or withd rawal , psychotic disorders, personality disorders
or malingering and factitious disorder.
• Through efficient, focused data gathering (which will frequently involve
interviewing other informants):
Determine which patients are at risk for the development of delirium.
Diagnose the underlying causes for delirium.
Contrast delirium and dementia (a potent risk factor for delirium);
categorise a sudden change in behaviour in a patient with dementia as
possible delirium superimposed on dementia.
• Interpret critical clinical and laboratory and mental state findings which
were key in the processes of exclusion, differentiation and diagnosis:
Select and interpret laboratory investigations in a patient with delirium.
List the indications for radiological imaging of the brain in a patient with
delirium.
• Conduct an effective plan of management for a patient with confusion/
delirium:
Outline the initial emergency management of patients with delirium
including protection of the patient from self-inflicted harm, harm to
others and methods to reduce disorientation and anxiety.
Describe the specific management of patients with delirium due to
hepatic encephalopathy, metabolic abnormalities and drugs.
Inform and support relatives.
120
023 Cyanosis/Hypoxaemia I Hypoxia
Overview
Cyanosis is the physical sign of hypoxaemia, but at times is difficult to detect (cyanosis
must be sought carefully, under proper lighting conditions). Hypoxaemia (low partial
pressure of oxygen in blood), when detected, may be reversible with oxygen therapy
after which the underlying cause requires diagnosis and management.
Causes
j1) Central cyanosis
a) Lung disease
0 Upper airway obstruction
0 Pulmonary embolism
0 Interstitial
• Infectious
• Inorganic dust (silicosis, asbestosis, coal, metals, etc.)
• Associated with other diseases (sarcoid, vasculitis, etc.)
• Chronic pulmonary oedema
• Idiopathic pulmonary fibrosis I fibrosing alveolitis
• Lymphangitic carcinomatosis
0 Chronic obstructive airways disease
b) Cyanotic heart disease
0 Eisenmenger syndrome (pulmonary hypertension with right-to-left
shunt)
0 Fallot tetralogy (ventricular septal defect (VSO); right ventricular
outflow obstruction; overriding aorta; right ventricular hypertrophy)
0 Transposition of great vessels
0 Total anomalous pulmonary venous drainage, truncus, single ventricle
I 2) Peripheral cya nosis

a) Low cardiac output
b) Local flow diminished (arterial/venous obstruction)
I 3) Localised cyanosis
121
Key Objectives
• Define cyanosis, hypoxaemia, and hypoxia (insufficient levels of oxygen in
tissues to maintain cell function) .
• Contrast pathophysiology of central and peripheral cyanosis .
Differentiate central cyanosis from peripheral and localised cyanosis .
Contrast respiratory causes and cyanotic congenital heart disease.
processes of exclusion, differentiation, and diagnosis.
• Conduct an effective plan of management for a patient with cyanosis/
hypoxaemia/hypoxia:
Outline an initial plan of management which includes treatment of the
underlying condition along with oxygen administration.
List the adverse effects of oxygen treatment.
List useful outcome criteria for a trial of long term use of oxygen in
patients with chronic hypoxaemia.
122
023 Cyanosis/Hypoxaemia I Hypoxia
023A Cyanosis I Hypoxia I Apnoea in Children
Overview
Evaluation of cyanosis and hypoxia in children depends heavily on the age of the child.
Cyanosis is an ominous finding, especially in the older child , and differentiation between
peripheral and central is essential in order to mount appropriate management.
Causes of cyanosis or hypoxaemia

1) Neonatal
a) Central
0 Cyanotic congenital heart disease
• Increased pulmonary blood flow (transposition, truncus arteriosus,
total anomalous pulmonary venous return , hypoplastic left heart)
• Obstruction to pulmonary blood flow (tricuspid, pulmonary atresia)
0 Respiratory insufficiency
• Pulmonary (respiratory distress syndrome, sepsis, aspiration,
diaphragmatic hernia)
• Central nervous system (CNS) (maternal sedative, asphyxia,
intracranial haemorrhage, hypoglycaemia)
b) Peripheral vascular ('physiologic acrocyanosis', sepsis, cardiogenic/
septic shock, thrombosis, vasomotor instability)
I 2) Infant and child

a) Central
0 Decreased oxygenation of haemoglobin
• Respiratory (pneumonia, cystic fibrosis, embolus, aspiration I
foreign body, CNS depression)
• Cardiac disease - cyanotic congenital heart disease, severe
congestive cardiac failu re (CCF) from any cause
0 Abnormalities of haemoglobin (methaemoglobinaemia)
b) Peripheral
0 Vascular problem (Raynaud disease, sepsis)
0 Obstruction (superior vena cava syndrome, deep venous thrombosis
(DVT))
0 Hyperviscosity (polycythaemia)
123
Key Objectives
• Differentiate between peripheral and central cyanosis since generalised
cyanosis is more consistent with primary heart disease or respiratory
insufficiency.
• Appreciate that if the process causing peripheral cyanosis is severe
enough (e.g. sepsis), generalised cyanosis may occur.
Elicit maternal history of illness or sepsis in pregnancy, gestational age,
delivery complications, presence of meconium, suction of infant, Apgar
score, family history of congenital heart disease.
Determine the vital signs, age of infant (ductus arteriosus usually closes
by third day), whether the infant is alert and active, if the infant is able to
feed, and the presence of respiratory distress (tachypnoea, grunting,
costal margin flaring or retraction) .
Perform examination of the newborn for evidence of respiratory
distress, congestive heart failure or shock, signs of CNS depression,
whether the cyanosis is central or peripheral.
Elicit history in the older child of acute versus chronic or recurrent
cyanosis, history of lung disease or heart disease, history of foreign
body or aspiration, fever, upper respiratory symptoms, exposure to
medications, dyes, chemicals.
In the older child, focus examination first on respiratory distress and
obtundation of neurologic disease; determine whether hypotension or
bradycardia is present (ominous signs).
Select laboratory investigations including diagnostic imaging,
electrocardiogram (ECG), and blood tests.
Explain the interpretation of hyperoxia test (arterial blood gas from a
site distal to the ductus on room air and 100% oxygen).
• Conduct an effective plan of management for a patient with cyanosis I
hypoxia I apnoea in children :
Outline initial management including cardio-respiratory monitoring.
Explain the benefit of 'knee-chest' position in a child with cyanosis and
tetralogy of Fallot.
124
024 Dementia I Memory Disturbances
Overview
Dementia is an acquired, progressive impairment of cognitive function characterised
by memory impairment, accompanied by other intellectual and personality changes, in
the setting of full consciousness. Dementia is a common problem, with most cases
being irreversible, the commonest cause being Alzheimer disease (more than 50% of
cases). Progress may be temporarily arrested or modified with specific treatments,
and potentially treatable causes must be sought.
Causes
1) Primary dementias (Alzheimer disease, Lewy body dementia,
Niemann-Pick disease, fronto-temporal dementia)
I 2) Vascular
a) Multi-infarct
b) Vasculitis I Autoimmune diseases
c) Focal subcortical strokes
13) Toxic
a) Alcohol, drugs and narcotics
b) Heavy metals I Dialysis dementia
c) Organic toxins
d) Carbon monoxide
4) Brain trauma (head injury, boxing, hypoxia)
5) Chronic infections (HIV, syphilis, Creutzfeldt..Jakob disease,

herpes simplex, malaria)
16) Mass lesions and/or neoplasms

a) Primary and secondary tumours, carcinomatous meningitis,
paraneoplastic encephalitis
b) Chronic subdural haematoma
c) Normal pressure hydrocephalus
I 7) Movement disorders
a) Parkinson disease
b) Huntington chorea
125
8) Endocrine, metabolic, and vitamin deficiency
a) Hypothyroidism/ Hyperthyroidism
b) Hypoparathyroidism/Hyperparathyroidism (HPT)
c) Hypoglycaemia/Hyperglycaemia (chronic)
d) Hypopituitarism
e) Pyridoxine, vitamin 8 12 and thiamin deficiency
I 9) Depressive pseudodementia
Key Objective
• Assess and identify treatable and reversible causes of cognitive
dysfunction, including the early stages of Alzheimer-type dementia.
• Through efficient, focused data gathering involving other informants as well
as the patient:
Establish the history of onset and progression of symptoms and current
level of functioning including daily living activities.
Conduct a baseline mental status assessment, including a Folstein
Mini-Mental State Examination (MMSE) and tests of frontal lobe
functioning.
Using the MMSE, differentiate depression or delirium from dementia.
Perform a comprehensive physical examination including neurological,
cardiovascular and endocrine systems and sensory impairments.
Categorise possible causes of dementia, and perform screening
investigations.
Identify and treat correctable conditions.
Know the indications for centrally acting cholinergic agents.
Determine the need for antidepressant or antipsychotic medication, or
psychiatric referral.
Assess and determine the role of the family or primary carer in the
support of the patient. Break the news sensitively.
Determine whether occupational and social or other therapy referral and
assessment is needed after considering the availability of community
resources.
126
• Conduct an effective plan of management for a patient with dementia with
memory/behaviour disturbances:
Outline management based on the patient's current and future levels of
disability, taking into account the wishes of the patient, the primary
carer/family, and available community resources.
Financial, legal and vehicle driving issues need to be considered.
Appreciate the indications, risk and benefits of the various psychotropic
agents which may be of value with specific symptoms.
Counsel and educate patients, carers and families about the natural
history of the disease and future care options.
Continue to provide support and advice to carers.
Consider end of life decisions and anticipate death and bereavement
issues.
12 7
025 Newborn in Poor Condition 1 Depressed Breathing
Overview
A call requesting assistance in the delivery room following the birth of a newborn may
be 'routine' or because the neonate is apparently depressed and requires resuscitation.
For any type of call, the doctor needs to be prepared to manage potential problems.
Causes
1) Respiratory problems
(see #023A Cyanosis/Hypoxia I Apnoea in Children)
a) Birth asphyxia or central nervous system (CNS) depression
(maternal drugs)
b) Meconium aspiration
c) Sepsis
d) Pneumothorax
2) Severe anaemia (erythroblastosis fetalis and secondary hydrops

fetalis)
I 3) Seizures
4) Congenital malformations including congenital heart disease J

birth injury
5) Shock - including that due to feto-maternal haemorrhage
6) Other (hypothermia, hypoglycaemia, small for dates neonate)
Key Objective
• Elicit selective maternal history, determine fetal vital signs, rapidly assess
for possible causes of the neonate's condition and initiate supportive
measures for the infant.
Elicit a maternal history including maternal illnesses, maternal use of
drugs, previous high-risk pregnancies, infections during pregnancy or
now, how long have membranes been ruptured, mother's blood type
and Ah status, evidence of polyhydramnios or oligohydramnios,
gestational age, any meconium, etc.
Identify significant causes of cardiorespiratory depression in the
newborn.
128
Outline the appropriate investigation of various causes of a 'depressed'
newborn and interpret the results.
• Conduct an effective plan of management for a 'depressed' newborn:
Differentiate management of respiratory failure in the presence and
absence of thick meconium.
Select patients in need of specialised care and initiate respiratory and
circulatory support prior to transfer of the infant for special care.
Counsel and provide explanation to family of the neonate's condition.
129
026 Development Disorder I Developmental Delay
(See also #014 Behaviour Disorder)
Ove rview
A clin ician is expected to assess development in an infant in order to diagnose
developmental delay.
Causes
1) Global delay
a) Environment (neglect, understimulation)
b) Chromosome disorders (e.g. trisomy 21 )
c) Genetic syndromes
d) Mental retardation, central nervous system (CNS) abnormalities
e) Inborn errors of metabolism I Hypothyroidism
12) Speech delay

a) Isolated speech delay
b) Sensory impairment (auditory/visual)
c) Autistic spectrum disorders (infantile autism)
3) Motor delay (Duchenne disease, cerebral palsy)
Key Objectives
• Using knowledge of normal child development, determine which chi ldren
have evidence of developmental delay.
• Determine whether the delay is global, isolated to speech/language or
motor delay, or includes abnormal social interaction.
Ge neral/Specific Objectives
Determine whether there is chronic illness, family history of
developmental delay, or risk factors for mental retardation.
Determine whether there was a congenital infection or HIV infection.
Determine whether there were factors predisposing to speech delay
(e.g. ototoxic drugs, recurrent otitis, mastoiditis).
Perform a developmental assessment to confirm or disprove
developmental delay.
130
Determine if there is reason to suspect child abuse or neglect.
List indications for referral for audiology assessment and referral to
speech and language pathologist.
• Conduct an effective plan of management for a patient with development
disorder I developmental delay:
Select children in need of specialised care.
Once a diagnosis of global delay is made outline for parents, along with
other caregivers, a management plan which includes (when
appropriate) medical care, multidisciplinary services, family support,
child placement, and academic support.
In a child with speech/language developmental delay, outline with the
assistance of specialised caregivers, a management plan which
includes (when appropriate) speech therapy, amplification devices,
family support, and educational modification.
131
027 Diarrhoea/Constipation
027A Acute Diarrhoea
Overview
Diarrhoeal diseases represent the second most common cause of death worldwide
and the leading cause of childhood death. Acute diarrhoea is defined as more than two
to three stools per day for up to three weeks. Chronic diarrhoea lasts over four weeks.
International travellers frequently suffer from acute attacks of diarrhoea in areas where
sanitation and hygiene are poor due to a variety of bacteria, viruses and parasites.
Causes
j 1) Dietary indiscretion
2) Laxatives (osmotic diarrhoea - e.g. magnesium sulphate,

lactulose)
I3) Infectious
a) Viral (rotavirus, cytomegalovirus (CMV), AIDS)
b) Travellers ' diarrhoea
0 Escherichia coli, enterotoxigenic
0 Escherichia coli, enteroadherent
0 Shigella, Salmonella
0 Protozoa (Amoebae, Giardia Iamblia)
(4) Food poisoning

a) Staphylococcus aureus
b) Escherichia coli
c) Shigella, Salmonella
d) Campylobacter, etc.
5) Post-antibiotic (e.g. Clostridium difficile

pseudomembranous colitis)
j 6) lschaemic
7) Inflammatory (exudative diarrhoea)

a) Inflammatory bowel disease (IBD)
132
Key Objectives
• Define the patient's precise diarrhoea with respect to the number of bowel
actions per day, the consistency, colou r and volume of stools and the
presence of other symptoms including blood, mucus or undigested food in
the faeces .
• Determine the time of onset and progress over time.
Differentiate infectious diarrhoea from IBD and other causes of acute
diarrhoea.
Select and interpret appropriate investigations for patients with acute
diarrhoea.
• Conduct an effective plan of management for a patient with blood in stool:
Outline management of patients with acute diarrhoea with attention to
public health concerns.
Select patients in need of specialised care and/or consultation.
Be aware of preventive measures to avoid traveller's diarrhoea and be
able to provide advice to travellers on steps to be taken in the event of
contracting a diarrhoeal illness.
133
0278 Chronic Diarrhoea
Overview
Patients with inflammatory bowel disease (IBD), especially ulcerative colitis, are at risk
for a variety of serious complications; patients with fatty stools suffer from malabsorption
of nutrients. An organised approach to the investigation of patients with chronic diarrhoea
will result in early diagnosis and avoidance of serious nutritional deficiencies and/or
serious complications.
Causes
j1) Osmotic
a) Malabsorption
Small bowel disease (gluten-sensitive enteropathy (coeliac disease),
bile acid malabsorption, small bowel diverticulosis, neoplasms (villous
adenoma, lymphoma, carcinoma), Whipple disease, etc.)
0 Pancreatic disease (chronic pancreatitis, cystic fibrosis)
0 Drugs
0 Bowel resection
b) Specific food intolerance (lactase deficiency, fructose intolerance)
I 2) Secretory
a) Inflammatory/Exudative
0 Bleeding
• Ulcerative colitis
• Chronic bacterial infection
Non-bleeding
• Crohn disease
• AIDS, tuberculosis (TB)
• Neoplasms (villous adenoma,
lymphoma)
b) Endocrinopathies (carcinoid, Ulcerative colitis
Zollinger-EIIison syndrome, VIPomas)
3) Motility (bacterial overgrowth, diabetic neuropathy,

scleroderma, short gut, etc.)
14) Irritable bowel syndrome
5) Spurious diarrhoea (faecal impaction)
134
Crohn enteritis
Crohn colitis
Key Objectives
• Differentiate true diarrhoea from spurious diarrhoea associated with faecal
impaction.
• Differentiate osmotic from secretory diarrhoea, and malabsorptive
diarrhoea from inflammatory causes.
Diagnose patients with irritable bowel syndrome.
Determine whether motility problems might be present.
Select and interpret investigations for malabsorptive conditions.
Select and interpret investigations for inflammatory bowel conditions.
• Conduct an effective plan of management for a patient with chronic
diarrhoea:
Outline plan of management for patients with chronic diarrhoea,
including the prevention and treatment of related complications {e.g.
patients with gluten-sensitive enteropathy, pancreatic insufficiency,
vitamin and mineral deficiencies).
Select patients in need of specialised care and/or consultation with
other healthcare professionals.
Conduct education and counselling of patients with malabsorption and
lBO.
135
027C Constipation/Encopresis, Paediatric
Overview
Constipation is a common problem in children . It is important to differentiate functional
from organic causes in order to develop appropriate management plans.
Causes
1) Psychologic/Developmental delay I Bedridden
2) Diet (inadequate fibre, excessive cow milk, undernutrition,

decreased fluid intake)
j 3) Anatomic
a) Hirschsprung disease
b) Anal stenosis I Atresia I
Imperforate anus
c) Mechanical obstruction/
malrotation
d) Absent/Abnormal abdominal
musculature ('prune belly')
I 4) Endocrine 1 Metabolic
a) Hypothyroid
b) Hypercalcaemia/Hypokalaemia
I 5) Neuromuscular
a) Cerebral palsy
b) Spinal cord disorders I Hlrschsprung disease
Meningomyelocele
c) Peripheral nerves (to gut)
d) Systemic striated I Enteric smooth myopathy
I 6) Medications
136
Key Objectives
• Determine whether the constipation should be investigated to exclude a
serious organic cause or should be managed symptomatically.
• Select patients with stool soiling or encopresis in need of investigation and
management.
Identify clinical features that help to distinguish functional from organic
causes of constipation.
Perform rectal examination on a child with minimal discomfort.
Evaluate the social and psychologic effects of chronic constipation and
chronic encopresis.
List appropriate investigation for chronic constipation.
• Conduct an effective plan of management for a patient with constipation:
Outline initial and long term therapy for constipation and encopresis,
including diet and education.
Identify children who require special, as opposed to conservative
management.
137
0270 Diarrhoea, Paediatric
Overview
Diarrhoea is defined as frequent, watery stools and is a com mon problem in infants
and children. In most cases, it is mild and self-limited. However, the potential for
hypovolaemia and electrolyte disturbance is ever present and may lead to significant
morbidity or even mortality.
Causes
1) Acute
a) Viral gastroenteritis (rotavirus, Norwalk, adenovirus, influenza,
enterovirus)
b) Bacterial colitis (Salmonella, Shigella, Yersinia, Campylobacter,
Escherichia coli)
c) Other infections (Clostridium difficile, giardiasis, amoebiasis,
parasites)
d) Food poisoning
I2) Malabsorption
a) Lactase deficiency
b) Cystic fibrosis
c) Coeliac disease
d) Primary immunodeficiencies (including HIV)
3) In the neonate (milk protein intolerance, necrotising

enterocolitis, overfeeding)
4) Other (drugs, laxative abuse, inflammatory bowel

disease (IBD), etc.)
138
Key Objective
• Determine the presence, degree and type of dehydration/volume depletion
and investigate the possibility of electrolyte abnormalities (see #009
Abnormal Serum Sodium Concentration, #008 Abnormal Serum Potassium
Concentration I Magnesium).
Elicit a history including previous weight, urine output, and associated
symptoms; examine vital signs, mucous membranes, skin turgor,
temperature of extremities, and fontanelle in infants, as well as
clubbing, wheezing , abdominal examination, etc.
Determine whether others have developed diarrhoea and whether the
onset was the same day as the ingestion of the same food or 24 hours
to days later.
Elicit a history of onset and duration of diarrhoea, stool pattern,
aggravating and alleviating factors, stool description, fever or
associated symptoms, diet history and travel history, etc. in order to
diagnose the aetiology of diarrhoea.
Select blood and stool investigations in patients with diarrhoea; interpret
electrolyte abnormalities.
Outline investigation of chronic diarrhoea.
• Conduct an effective plan of management for a young patient with
diarrhoea:
Outline treatment for the underlying cause of the diarrhoea.
Select patients who require referral to a nutrition expert (e.g.
malabsorption, coeliac disease).
Outline supportive management for patients with volume and/or
electrolyte disorders.
Discuss nutritional rehabilitation in a malnourished patient.
Discuss the use of community resources for parental support.
Notify the local public health authority if appropriate .
139
- - - ---- --- - - - - -
027E Adult Constipation
Overview
Constipation is the infrequent passage of stools or of stools that are harder and more
difficult to pass than the individual's normal bowel pattern. Low-fibre diets and lack of
activity may worsen constipation. Chronic constipation often follows the habitual ignoring
of the stimulus to defaecate. Constipation is an important symptom of colon cancer;
colonic malignancy is one of the most common causes of mechanical intestinal
obstruction.
Causes
1) Simple constipation
a) Low dietary fibre
b) Functional (environment/diet or fluid consumption I activity level
change)
I 2) Disordered motility
a) Irritable bowel syndrome
b) Diverticular disease I 'Obstipation ' I Faecal impaction
c) Idiopathic slow transit
I 3) Secondary constipation
a) Local ano-recta l problems (anal fissure/stricture/haemorrhoids)
b) Drugs (opioid analgesics, chronic laxatives, cough medicine, iron,
calcium , calcium channel blockers, other antihypertensive drugs,
etc.)
c) Prolonged immobilisation
140
- --- - - - - -- - - - - - - - - - ---
027E Adult Constipation
Overview
Constipation is the infrequent passage of stools or of stools that are harder and more
difficult to pass than the individual's normal bowel pattern. Low-fibre diets and lack of
activity may worsen constipation. Chronic constipation often follows the habitual ignoring
of the stimulus to defaecate. Constipation is an important symptom of colon cancer;
colonic malignancy is one of the most common causes of mechanical intestinal
obstruction.
Causes
1) Simple constipation
a) Low dietary fibre
b) Functional (environment/diet or fluid consumption I activity level
change)
I2) Disordered motility

a) Irritable bowel syndrome
b) Diverticular disease I 'Obstipation' I Faecal impaction
c) Idiopathic slow transit
I 3) Secondary constipation
a) Local ano-rectal problems (anal fissure/stricture/haemorrhoids)
b) Drugs (opioid analgesics, chronic laxatives, cough medicine, iron,
calcium , calcium channel blockers, other antihypertensive drugs,
etc.)
c) Prolonged immobilisation
140
d) Bowel tumours (rectal, colonic)
e) Metabolic disorders I Pregnancy (diabetes, hypercalcaemia,
hypothyroidism)
f) Neurological disorders (Hirschsprung disease, spinal cord disease)
g) Bowel obstruction (see #001 Abdominal Distension / Ileus)
Distended caecum -large bowel obstruction
Key Objectives
• Appreciate that constipation is usually related to influences of diet and
activity.
• Appreciate when constipation should be investigated for a serious cause or
should be managed symptomatically.
• In a patient with constipation:
Be able to take an appropriate history and undertake a relevant physical
examination.
Remember to do a rectal examination.
• Appreciate the likelihood that the patient's symptoms may be due to
malignancy.
• Understand the place of investigations in diagnosis and management.
• Interpret critical cl inical and laboratory findings which were key in the
Select and interpret investigations including stool for occult blood, and
select patients in need of examination by endoscopy or diagnostic
imaging.
• Conduct an effective plan of management for a patient with constipation:
Outline a plan of management for simple constipation and for
constipation due to disordered motility.
141
028 Diplopia (Double Vision)
Overview
Disorders of eye movement usually present with diplopia. Monocular diplopia (diplopia
persisting with occlusion of vision to the other sound eye) is almost always indicative of
relatively benign optical problems whereas binocular diplopia is due to ocular
misalignment. Once restrictive disease or myasthenia gravis is excluded, the major
cause of binocular diplopia is a cranial nerve lesion. Careful clinical assessment is
necessary for appropriate management.
Causes
1) Monocular diplopia (refractive error, keratoconus,
cataract, functional)
I 2) Binocular diplopia
a) Oculomotor nerves
0 Third nerve (ischaemia, especially diabetes-associated, aneurysm,
tumour, trauma)
0 Fourth nerve (ischaemia, especially diabetes-associated , trauma)
0 Sixth nerve (ischaemia, especially diabetes-associated, tumour,
subdural haematoma, trauma)
{in children consider also postviral inflammation, brain stem tumour}
b) Myoneural junction (myasthenia gravis)
c) Extraocular muscles
restriction/entrapment
0 Exophthalmos
0 Orbital inflammation
0 Orbital tumour
0 Fracture of the orbital floor
('blowout' fracture)
__
......_
Left 6th nerve palsy - strabismus with
diplopia
......; on left lateral gaze
142
Key Objectives
• Determine whether the rare condition of monocular diplopia is present or
the diplopia is binocular (resolves with occlusion of vision to either eye).
• Determine whether the cause of binocular diplopia is a cranial nerve lesion,
which may be the first presentation of a life-threatening condition .
Determine whether restrictive disease, oculomotor nerve palsy or
myasthenia gravis is the likely cause of diplopia; determine whether one
pupil is dilated in a patient with third nerve palsy (suggestive of
aneurysm in circle of Willis).
Determine whether doubling of images occurred suddenly (acute event
such as ischaemia) or is gradually worsening (progressive process such
as tumour or inflammation).
Describe the mechanism of development of the 'down and out' eye in a
third nerve lesion.
Describe findings expected in fourth and sixth nerve lesions.
Describe the value of the Tensilon test for myasthenia gravis.
List indications for angiography or computed tomography (CT) I
magnetic resonance imaging (MAl).
• Develop an effective plan of management and referral for patients with
diplopia.
143
029 Dizziness/Vertigo
Overview
True vertigo (an episodic sensation of rotation of the body or its surroundings) must be
distinguished from dizziness or pseudovertigo (light-headedness, giddiness, faintness,
unsteadiness) because it indicates the presence of localised, rather than generalised,
pathology. Some causes of vertigo are serious. Others can be chronic and difficult to
treat.
Causes
1) True vertigo
a) Peripheral (labyrinth or acoustic nerve)
0 Motion sickness
0 Benign positional vertigo
0 Acute labyrinthitis
0 Vestibular neuronitis
0 Meniere disease
0 Acoustic neuroma (Schwannoma)
0 Chronic otitis media
0 Alcohol
0 Drugs prescribed or self-admin istered
0 Illicit drugs
0 Trauma
0 Wax in ear canal
b) Central (brainstem or cerebellum)
0 Vertebrobasilar insufficiency
0 Cerebellar artery syndrome
0 Infarct
0 Tumour (primary or secondary)
0 Migraine
0 Multiple sclerosis
0 Head injury
12) Dizziness (pseudovertigo)

a) Postural hypotension
b) Hyperventilation
c) Syncope/Pre-syncope including vaso-vagal attack
d) Cardiac arrhythmias
e) Aortic stenosis
f) Acute myocardial infarction (MI)
144
g) Head injury
h) Hypoglycaemia
i) Alcohol and drugs
j) Anaemia
k) Psychogenic
I) Idiopathic (particularly in the elderly)
Key Objectives
• Determine whether patients complaining of dizziness have true vertigo or
pseudovertigo.
• Differentiate between central and peripheral causes for true vertigo.
• Identify and cou nsel patients with other causes of dizziness.
• Use of directed history-taking and regional examination, particularly
neurological examination and special office tests.
• Order and interpret the appropriate investigations used in the diagnosis of
patients with dizziness/vertigo.
• Conduct an effective plan of management for a patient with dizziness/
vertigo:
Determine which patients with vertigo require urgent investigation and
management.
Describe the symptomatic management of patients with benign causes
of vertigo.
Counsel and educate patients with benign causes of dizziness/vertigo.
145
030 Dying Patient
Overview
Doctors are frequently faced with patients dying from incurable disease. In such
circumstances, the most important roles of the doctor are to improve the quality of
remaining life by alleviating suffering by the patient, thereby facilitating a 'good death';
and to provide comfort and empathetic and compassionate support to patients and
their families.
Ke y Objective
• When caring for a dying patient, doctors must listen to what the patient
says are the primary concerns, and should formulate a management plan
that ensures adequate control of: pain; relief of anxiety and depression;
respect for patient autonomy and control ; maintenance of human dignity
and privacy. The plan should not prolong life pointlessly; and should avoid
isolation of the patient from family and loved ones.
• Through empathetic and efficient data gathering:
Discuss with patients their wishes for care in their final days.
For patients who are currently incompetent, insensible or unable to
express their wishes, determine whether an advanced directive was
previously written or expressed.
• Implement an effective plan of management for a dying patient which
includes:
Selecting analgesic dosages that are adequate for pain control and
alleviating dyspnoea in those who forego mechanical ventilation, even if
by doing so death is hastened.
Discussing with patients their wishes for care , including resuscitation,
well in advance of their death.
Discussing the role of an advanced directive and the impact this has on
clinicians.
Providing or arranging for psychosocial, emotional, practical, legal and
spiritual support to the patient and family.
Selecting patients in need of referral to other health professionals and
ensuring access to information and expertise of whatever kind is
necessary.
Educating patients and their families about the nature of the causal
condition and the process of dying.
Promoting active coping strategies when appropriate.
146
Gently facilitating and acknowledging the expression of feelings,
particularly anticipatory grief; and alleviating fear and depression with
appropriate treatments.
Being sensitive to the burden of care borne by others.
Encouraging the strengthening of relationships with loved ones.
Remembering the relevance of funerals as life-enhancing experiences.
147
031 Dysphagia
Overview
Dysphagia is a significant symptom that, if appropriately approached, will enable doctors
to distinguish between a benign or malignant cause. With more effective therapy for
gastro-oesophageal reflux disease and an increase in the incidence of oesophageal
cancer, the symptom of dysphagia is now more frequently an indication of malignant
oesophageal obstruction. Mechanical dysphagia thus represents carcinoma until proved
otherwise. Physical signs are usually few and appropriate endoscopic/radiologic
investigation is essential.
Dysphagia should be distinguished from the anxiety disorder globus hystericus (globus
disorder), which is the sensation of a constant irritating lump in the throat without
swallowing difficulty.
Causes
1) Oropharyngeal dysphagia (peritonsillar abscess,
pharyng~is,cancer,pharyngealpouch)
I 2) Oesophageal dysphagia
a) Mechanical obstruction
0 Carcinoma (squamous cell , adenocarcinoma)
0 Other causes (stricture (reflux oesophagitis, corrosives) ,
paraoesophageal hiatus hernia, foreign body, goitre, upper
oesophageal web (sideropenic dysphagia))
Para-oesophageal hiatus hernia
148
Sliding hiatus hernia with Achalasia
oesophagt!NII stricture
b) Neuromuscular/Motility disorder
f.J Intermittent (oesophageal spasm)
0 Progressive
• Achalasia
• Central nervous system (stroke, Parkinson disease, amyotrophic
lateral sclerosis, poliomyelitis, multiple sclerosis, pseudobulbar
palsy)
• Cranial nerves (diabetes, laryngeal nerve palsy)
• Skeletal muscle disease (poliomyelitis, dermatomyositis,
scleroderma)
Key Objectives
• Contrast difficulty initiating swallowing (coughing, choking , nasal
regurgitation) , from food sticking after being swallowed, and then
dysphagia involving only solid food from dysphagia of both solid and liquid
food, and whether intermittent or progressive.
• Distinguish between oropharyngeal and oesophageal dysphagia.
• Distinguish between difficu lty in swallowing and pain on swallowing.
Determine whether symptomatology is intermittent or progressive,
whether weight loss (late sign) is a problem, and whether any
neurologic symptom or aspiration coexists.
Determine the presence of coughing, choking, drooling, or regurgitation.
Select patients in need of specialised investigative procedures (e.g.
endoscopy); if not available, select diagnostic imaging.
• Conduct an effective plan of management for a patient with dysphagia:
Select patients in need of specialised care and/or referral.
149
032 Dyspnoea and/or Cough I Prevention of Cancers
and Chronic Respiratory Diseases
Overview
Shortness of breath may be due to a variety of causes. It is imperative to identify
rapidly the aetiology in order to mount, if required , an immediate and long term
management programme to minimise complications and excessive morbidity.
Causes
1) Upper airway
a) Stridor
I2) Lower airway

a) Obstructive (asthma, chronic obstructive lung disease, inhaled
foreign body)
b) Non-obstructive (interstitial lung disease, restrictive lung disease)
13) Cardiac causes

a) Left heart failure
b) Aortic stenosis
4) Pneumothorax
5) Pulmonary embolism
6) Pleural effusion
7) Psychogenic
8) Severe anaemia
9) Metabolic acidosis
10) Central nervous system (CNS)
11) Musculoskeletal
Key Objectives
• Differentiate dyspnoea from tachypnoea, hyperpnoea or hypeNentilation.
• Differentiate cardiac from pulmonary, neuromuscular or other causes of
dyspnoea.
• Develop management programmes to treat the immediate problem and
involve the patient, the family and community resources in the overall care
of chronic patients.
150
Differentiate between the causes of cardiac pulmonary oedema.
Differentiate between the various causes of pulmonary oedema and
pulmonary infiltrations.
Diagnose the various causes of life-threatening dyspnoea.
Appropriately select and interpret lung imaging.
Appropriately select and interpret cardiac-related investigations.
• Conduct an effective plan of management for a young patient with
dyspnoea:
Outline initial management for patients with acute dyspnoea of cardiac,
pulmonary, or other origins.
Select patients in need of specialised care and referral to other
healthcare professionals or institutions.
Select those patients in need of hospitalisation.
Conduct appropriate education of patients including secondary
prevention strategies.
151
032 Dyspnoea and/ or Cough I Prevention of Cancers
032A With Diffuse Chest X-Ray Abnormality
Overview
Shortness of breath has many causes. Prompt recogn ition of the diagnosis and initiation
of therapy can limit associated morbidity and mortality.
Causes
11) Cardiac causes - pulmonary oedema

a) Cardiomyopathy
0 lschaemic
Dilated (idiopathic, alcoholic,
haemochromatosis)
b) Hypertensive heart disease
c) Restrictive cardiomyopathy
(amyloid, sarcoid)
d) Valvular heart disease
e) Diastolic dysfunction (hypertension,
ischaemia, infiltrative disease)
f) Increased cardiac output (anaemia,
arteriovenous (AV) malformation,
hyperthyroid)
Mitral regurgitation
12) Pulmonary Causes
a) Infectious Pneumonia
0 Bacterial, including tuberculosis (TB)
:..J Atypical
':1 Fungal, including Pneumocystis carinii
Viral, including HIV
b) lnhalationai/Environmental
'pneumoconiosis'
(inorganic, organic)
c) Vasculitis (Wegener
.
.. ,,
granulomatosis,
Goodpasture syndrome)
d) Pulmonary fibrosis,
sarcoidosis, scleroderma
Pneumococcal pneumonia
152
e) Neoplastic (lymphangitic carcinomatosis)
f) Drugs/Radiation (amiodarone, bleomycin, beta-blockers,
nitrofurantoin)
Lymphangltic carcinoma Pneumocystis pneumonia
Key Objectives
• Differentiate true cough from upper airway clearing , saliva from sputum or
haemoptysis, and true dyspnoea from tachypnoea, hyperpnoea, and
hyperventilation.
• If initial evaluation indicated that a chest X-ray was necessary, differentiate
between cardiac disease, pulmonary disease, and neuropsychiatric
disease.
Differentiate between causes of cardiac pulmonary oedema.
Differentiate between causes of pulmonary disease.
Diagnose acute, life-threatening dyspnoea.
processes of exclusion, differentiation. and diagnosis:
Select and interpret lung imaging.
Select and interpret heart-related investigations.
• Conduct an effective plan of management for a patient with cough and/or
dyspnoea with diffuse chest X-ray abnormality:
Outline initial management for patients with acute dyspnoea of cardiac,
pulmonary, or neuropsychiatric origin.
Select patients in need of specialised care and referral to other
healthcare professionals.
Select patients requiring hospitalisation.
Conduct appropriate education of patients including secondary
prevention strategies.
153
0328 With Pleural Chest X-Ray Abnormality
Overview
Pleural effusions are common and may represent local or systemic disease.
Causes
11) Pleural effusion
a) Exudative
0 Neoplastic causes
0 Infectious causes
• Parapneumonic
• Empyema (bacterial, fungal,
tubercu lous)
0 Pulmonary emboli
0 Collagen-vascular diseases (rheumatoid,
lupus pleuritis)
0 Gastrointestinal causes (ruptured
oesophagus, pancreatitis)
b) Transudative
0 Congestive heart failure
Cirrhosis
0 Nephrotic syndrome
0 Pulmonary emboli
I2) Pleural thickening

a) Chronic infections (tuberculosis (TB))
b) Neoplastic (mesothelioma)
c) Inflammatory (chronic asbestos
exposure)
I 3) Pneumothorax
a) Spontaneous
0 Primary
0 Secondary (secondary to chronic
obstructive pulmonary disease Right pneumothorax
(COPD))
b) Traumatic
c) Tension
154
Key Objectives
• Conduct an examination of the thorax and demonstrate how to detect a
pleural effusion or a pneumothorax; identify life-threatening tension
pneumothorax requiring urgent treatment.
• Differentiate between causes of pleural effusion on the basis of analysis
results from pleural fluid .
Differentiate between a pleural effusion and a pneumothorax.
Perform intercostal needle thoracentesis as initial life-saving procedure
for tension pneumothorax; arrange for subsequent intercostal tube
thoracentesis.
Interpret the findings of a chest X-ray.
Perform (under supervision) and interpret the findings of a
thoracocentesis and intercostal catheter insertion; appreciate hazards
of procedure and methods of prevention of complications.
Discuss the indications for computed tomography (CT) scanning in
patients with a pleural effusion.
• Conduct an effective plan of management for a patient with dyspnoea and/
or cough with pleural chest X-ray abnormality:
Identify patients in need of immediate management for pneumothorax.
Discuss the medical and surgical management for patients with pleural
effusion.
188
032C With Fever
Overview
Cough with fever may signify pneumonia that can result in rapid deterioration of health.
Prompt management of patients with pneumonia may be life-saving.
Causes
1) Infectious causes
a) Bronchitis (bacterial or viral)
b) Pneumonia
Bacterial (typical, atypical)
0 Viral (including severe acute respiratory syndrome (SARS)
viral pneumonia)
0 Tuberculous or fungal
c) Upper respiratory tract infections (URTis)
2) Inflammatory causes (e.g. pulmonary vasculitis)
13) Pulmonary embolus
14) Neoplastic causes

a) Primary
b) Secondary
Interstitial pneumonia
156
Key Objective
• Determine which patients with dyspnoea, cough and fever are likely to have
serious pulmonary disease and require immediate investigation and prompt
management.
Diagnose the cause of dyspnoea, cough and fever.
For patients with pneumonia, elicit risk factors which predispose such
patients to specific organisms.
Determine which patients are at risk for fungal pneumonia or tuberculosis
(TB).
Order and interpret the results of a chest X-ray in patients with cough
and fever.
Order and interpret the results of microbiological cultures and viral
serology if appropriate.
or cough with fever:
Assess the severity of the illness and discuss the indications for
hospitalisation and referral to specialised care .
Discuss the indications for anti-microbial therapy and select the most
appropriate antibiotic based on the likelihood of infection with specific
micro-organisms.
Discuss the treatment and followup of patients with TB.
Discuss the preventive and public health measures related to
pulmonary infections including TB.
157
0320 With Local Chest X-Ray Abnormality
Overview
Dyspnoea and cough with an abnormal chest X-ray are indicative of significant pathology.
Accurate interpretation of the chest X-ray is critical for making a diaQnosis.
Causes
11) Infectious causes
a) Pneumonia
0 Bacterial (typical, atypical)
0 Viral
0 Tuberculous
0 Fungal
0 Parasitic (hydatid cyst)
b) Lung abscess (bacterial or tuberculous) Hydatid cyst of lung
12) Neoplasm
a) Benign (hamartoma, granuloma)
b) Malignant
0 Primary (small cell, non-small cell
lung cancer)
0 Secondary (metastases, lymphoma)
13) Interstitial lung disease

(see #032A With Diffuse Chest X-Ray
Abnormality)
a) lnhalationai/Environmental Lung cancer
0 Inorganic (silicosis, asbestosis, coal
worker's pneumoconiosis, etc.)
0 Organic (extrinsic allergic alveolitis)
b) Collagen vascular diseases (systemic
lupus erythematosus (SLE), rheumatoid
arthritis (RA), ankylosing spondylitis
and polymyositis)
c) Drug/Radiation induced (amiodarone,
bleomycin, nitrofurantoin)
d) Idiopathic (pulmonary fibrosis, sarcoidosis)
Lymphoma
e) Vasculitis (Wegener granulomatosis)
158
Right middle lobe Lung metastasis -
collapse renal primary
14) Mediastinal masses
a) Anterior (thymomas, lymphoma, thyroid mass, teratoma)

b) Middle and posterior (unlikely to present with dyspnoea/cough)
Is) Miscellaneous
a) Atelectasis I Pulmonary collapse
b) Loculated pleural effusion
Key Objective
• Differentiate patients with infectious or neoplastic causes for their dyspnoea
and/or cough and chest X-ray abnormality.
Diagnose the cause of dyspnoea and/or cough and localised chest
X-ray abnormality.
Determine the most likely cause for interstitial lung disease.
In patients with pulmonary nodules, describe risk factors and clinical
features favouring malignancy.
List indications for chest computed tomography (CT) scan in patients
with dyspnoea, cough and a localised X-ray abnormality.
Discuss investigation for patients with a pulmonary nodule.
Describe chest X-ray features of pulmonary nodules favouring
malignancy.
or cough with a local chest X-ray abnormality:
Assess the severity of illness and discuss the indications for
hospitalisation and referral for specialised care.
Describe a management plan based on the mostly likely cause of the
chest X-ray abnormality.
159
032 Dyspnoea and/or Cough 1 Prevention of Cancers
032E With Normal Chest X-Ray
Overview
Since patients with acute dyspnoea require more immediate evaluation and treatment,
it is important to differentiate them from those with chronic dyspnoea.
Causes
l1) Acute dyspnoea

a) Exacerbation of obstructive airways disease
0 Asthma
0 Chronic obstructive pulmonary disease (COPD)
b) Pulmonary embolus
c) Early pneumonia
d) Miscellaneous (anxiety, fever, sepsis, salicylate, metabolic acidosis)
I 2) Chronic dyspnoea
a) Obstructive airways disease
0 Asthma
0 COPD
0 Bronchiectasis
b) Chronic congestive heart failure
c) Neuromuscular disorders (post-poliomyelitis, myasthenia gravis,
muscular dystrophy)
Key Objective
• Differentiate clinically among the causes for acute and chronic dyspnoea.
Differentiate between the different causes for obstructive airways
disease.
Determine which factors may precipitate dyspnoeic episodes in patients
with asthma or chronic obstructive lung disease.
160
Order and interpret appropriate initial investigations including chest
X-ray, arterial blood gas and pulmonary function tests.
Outline the diagnostic imaging appropriate for a patient with suspected
pulmonary embolus.
or cough with a normal chest X-ray:
Determine which patients have life-threatening acute dyspnoea and
perform immediate management, including intubation if necessary.
Discuss the acute and chronic pharmacological management of
patients with obstructive airways disease.
Select patients in need of hospitalisation and/or specialised care.
Counsel and educate patients in strategies for smoking cessation and
avoidance of precipitants.
Describe the complications of chronic hypoxia and hypercapnia and
outline the role of oxygen supplementation in patients with chronic
hypoxia.
161
032F Cough
Overview
Chronic cough is one of the most common symptoms for which patients seek medical
advice. Assessment of chronic cough must be thorough. Patients with benign causes
for their cough (e.g. gastro-oesophageal reflux, post-nasal drip, two of the commonest
causes) can often be effectively and easily managed. Patients with more serious causes
for their cough (e.g. asthma, the other common cause of chronic cough) require full
investigation, and management is more complex.
Causes
1) Chronic cough
a) Miscellaneous
0 Post-nasal drip
0 Gastro-oesophageal reflux
0 Drugs (angiotensin-converting enzyme (ACE) inhibitors)
0 Foreign body
0 Chronic sinusitis
b) Obstructive airways disease
0 Asthma
0 Chronic bronchitis
0 Bronchiectasis
0 Cystic fibrosis
c) Congestive heart failure
d) Lung neoplasm
0 Bronchogenic carcinoma
0 Carcinoid tumour
e) Chronic lung infections
0 Lung abscess
0 Tuberculosis (TB)
f) Interstitial lung disease
162
2) Acute cough
a) Infectious (upper respiratory tract infection (URTI), bronchitis,
pneumonia)
b) Irritant (noxious fumes, smoke)
Bilateral pneumonia
Key Objective
• Differentiate patients with chronic cough due to upper or lower respiratory,
cardiac or gastrointestinal causes.
Determine whether the patient smokes or takes ACE inhibitors (if not,
consider reflux or post-nasal drip).
Diagnose the cause of a chronic cough and distinguish those patients
with innocuous cough from those with significant disease.
Outline value of spirometry before and after broncho-dilators for
assessment of chronic cough.
Order and interpret a chest X-ray if appropriate.
• Conduct an effective plan of management for a patient with a chronic
cough:
Prescribe appropriate medications used in the management of chronic
cough , with proper attention to their indications, contra-indications and
adverse effects.
Counsel and educate patients with chronic cough including the
provision of strategies aimed at smoking cessation.
183
032G Dyspnoea 1 Respiratory Distress, Paediatric
Overview
Respiratory distress is one of the most common paediatric emergencies and can be a
life-threatening acute emergency.
Causes
l1) Airway problems
a) ' Croup' (acute laryngotracheobronchitis)
b) Foreign body aspiration
c) Laryngeal oedema I Spasm I Epiglottitis
d) Retropharyngeal abscess
I 2) Pulmonary problems
a) Tracheitis/Bronchiolitis
b) Pneumonia
c) Asthma/Bronchospasm
I3) Cardiac problems

a) Congestive heart failure (left-to-right shunt, left ventricular failure)
b) Cardiac tamponade
c) Pulmonary embolus
14) Pleural problems

a) Pleural effusion, empyema
b) Pneumothorax
5) Neurologic problems (opiates, increased intracranial

pressure, neuromyopathic)
I 6) Neonatal conditions
a) Transient tachypnoea of the newborn
b) Respiratory distress syndrome (hyaline membrane disease)
c) Diaphragmatic hernia
d) Massive ascites
e) Trachea-oesophageal fistula
17) Other (e.g. severe scoliosis)
164
Key Objectives
• Differentiate the child who appears well from a child in distress or in critical
condition.
• Evaluate the respiratory rate in the context of age of the child (neonates
normally breathe 35- 50 times per minute, infants 30-40, elementary school
children 20-30, and pre-adolescents 12-20) and describe and explain the
quality of the breathing.
• Differentiate dyspnoea from tachypnoea, hyperpnoea or hyperventilation.
Differentiate the child who appears well from a child in distress or in
critical condition.
Ensure patent airway.
Determine presence, duration, and type of onset of respiratory distress,
presence of cyanosis.
Perform examination for vital signs, retraction, flaring, wheezing , or
coughing.
Perform examination - cyanosis, upper airway, heart, lungs and other
relevant areas.
Assess pulse oximetry.
Determine presence of hypoxia; select and interpret lung imaging and/
or cardiac investigations.
Outline other tests of blood, sputum, electrocardiogram (ECG),
echocardiography, etc. as appropriate. Special tests may be required if
patient is immune-compromised.
• Conduct an effective plan of management for a patient in respiratory
distress:
Outline immediate management of hypoxia; select patients in need of
hospitalisation/referral .
Discuss potential side-effects of oxygen therapy.
Explain choice of antibiotics for pulmonary disorders; discuss use of
bronchodilators and steroids if appropriate.
Explain advantages/disadvantages of diuretics (e.g. frusemide) in the
treatment of cardiac dyspnoea.
Counsel patients/parents about secondary prevention strategies.
165
033 Ear Pain
Overview
Many causes of ear pain exist but acute otitis media is by far the most common,
especially in children. Diagnosis and treatment of otitis media is usually straightforward
but other causes may present more difficult management situations.
Causes
11) Pinna
a) Cellulitis/Perichondritis
b) Chilblains
c) Trauma
2) External auditory meatus and ear canal

a) Impacted wax I foreign body
b) Furunculosis
c) Otitis externa
d) Herpes zoster- geniculate herpes (Ramsay Hunt syndrome)
e) Tumour (basal cell carcinoma (BCC), squamous cell carcinoma
(SCC), osteoma)
I 3) Middle Ear
a) Acute otitis media
b) Eustachian obstruction
c) Barotrauma
d) Acute mastoiditis
e) Chronic otitis media and cholesteatoma
f) Penetrating injury
14) Peri-otic
a) Temporomandibular joint (TMJ) dysfunction
b) Impacted wisdom teeth
c) Parotitis
d) Temporal arteritis
e) Erysipelas
f) Pharyngitis/Tonsillitis
166
I 5) Referred Pain
a) Cervical adenitis
b) Upper cervical spine disorder
c) Glossopharyngeal neuralgia
d) Thyroiditis
e) Laryngeal/Pharyngeal tumours
Key Objectives
• Skill in examination of the ear canal and tympanic membrane using an
auroscope.
• Identification of diagnostic features of otitis media, and knowledge of the
treatment of acute otitis media.
• Identification and management of other causes of ear pain.
Localise the site of pain.
Systematically examine structures which may be the source of origin of
the pain.
Differentiate between localised and referred pain.
• Interpret critical clinical findings and investigations which were key in the
process of exclusion, differentiation and diagnosis:
Select any necessary investigation which will confirm, exclude or
suggest a possible cause of the ear pain.
• Conduct an effective plan of management for a patient with ear pain:
Specific treatments for infective causes.
Minor procedures for mechanical causes.
167
034 Oedema
034A Generalised Oedema
Overview
Patients frequently complain of generalised swelling or bloating. At times, the swelling
may be caused by relatively benign conditions, but at times, serious underlying diseases
may be present.
Causes
11) Idiopathic (cyclical oedema)
12) Drugs
a) Causing fluid retention (minoxidil, nonsteroidal anti-inflammatory
drugs (NSAIDs), etc.)
b) Without fluid retention (calcium channel blockers, especially
dihydropyridines)
l 3) Cardiac failure
4) Nephrotic syndrome (and/or severe hypoalbuminaemia)
I 5) Liver failure
I 6) Renal failure
Key Objective
• Differentiate systemic generalised oedema from localised oedema;
categorise oedema as 'underfill' or 'overfill' based on patient's volume
status, since management may be affected.
Differentiate between the various causes of systemic oedema.
Select and interpret laboratory investigations for oedema.
168
• Conduct an effective plan of management for a patient with generalised
oedema:
Outline a plan of management for oedema of varying causes.
List appropriate dietary interventions.
List complications of diuretic use; contrast diuretic use in 'underfill'
versus 'overfill' oedema.
169
034 Oedema
0348 Unilateral Limb Oedema (Swollen Limb}
Overview
The most common causes of unilateral leg oedema are trauma, infection, venous disease
and chronic lymphoedema. The ability to reach a diagnosis requires good clinical skills;
the most important conditions not to miss are cellulitis and deep venous thrombosis
(DVT).
Causes
1) Muscle strain, tear, twisting injury to extremity, haematoma
12) DVT
a) Lower extremity (proximal, calf vein)
b) Upper extremity (effort thrombosis, central venous cannulation ,
chemotherapy)
I 3) Infection/Inflammation
a) Cellulitis I Soft tissue I Bone
b) Chronic dermatitis I Cutaneous mucinosis
14) Venous insufficiency
5) Lymphatic obstruction J Lymphangitis
I 6) Baker cyst
7) Infiltrative dermopathy (usually associated with thyroid disease)
Key Objectives
• Diagnose proximal lower extremity DVT with accuracy and certainty since
untreated, it may lead to pulmonary embolus, and treatment with
anticoagulants is associated with significant risk.
• Diagnose cellulitis with accuracy and certainty since early and adequate
antibiotic treatment is required to prevent serious complications.
Elicit history of predisposing factors, particularly for DVT and cellulitis.
Be aware of the key risk factors for DVT (immobilisation, surgery,
obesity, previous episode of thrombosis, varicose veins, trauma,
malignancy, postpartum, oestrogen therapy, a thrombophilia or family
history of thrombosis) .
170
Examine extremity for tenderness, presence or absence of pitting
oedema, inflammation, discolouration, palpable cord, skin changes,
venous ulceration, and especially arterial blood supply.
State that clinical diagnosis of DVT is not sufficiently accurate, and
diagnostic tests are indicated to confirm or exclude the diagnosis.
Discuss D-dimer measurements, and compression ultrasound and
compare to contrast venography.
Select duplex ultrasonography Doppler for the diagnosis of chronic
venous insufficiency.
• Conduct an effective plan of management for a patient with oedema which
is not generalised:
Outline primary prevention and management of DVT.
Outline the management of cellulitis.
List indications, compl ications and management of anticoagulant
therapy.
Counsel patients about anticoagulant therapy.
Streptococcal cellulitis Lymphoedema - cellulitis
171
035 Eye Redness
Overview
Red eye is a very common complaint, and despite the rather lengthy list of causal
conditions , three problems make up the vast majority of causes: conjunctivitis, foreign
body, and iritis (uveitis). The most common cause is conjunctivitis. If unilateral and
painful a serious cause is more likely - beware of the unilateral painful red eye!
Causes
1) Lids I Orbits 1 Lacrimal syste m
a) Foreign body
b) Hordeolum ('stye')
c) Chalazion (Meibomian cyst)
d) Blepharitis
e) Cellulitis (anterior, posterior)
f) Naso-lacrimal duct obstruction/ 'Stye' - infected eyelash
dysfunction
g) Orbital cellulitis
12) Conjunctiva
a) Conjunctivitis
u Viral
0 Bacterial (including
gonorrhoea and trachoma in
the neonate)
0 Fungal
0 Allergic
b) Pinguecula/Pterygium
c) Dry eyes
d) Subconjunctival haemorrhage
3) Cornea
a) Corneal abrasion
b) Corneal foreign body
c) Corneal ulcer
d) Herpes simplex keratitis
(dendritic ulcer)
e) Herpes zoster ophthalmicus
f) Fungal keratitis
172
I4) Anterior chamber
a) Acute glaucoma
b) Acute iritis (iridocyclitis, uveitis)
c) Choroiditis
d) Hyphaema
is) Whole eye

a) Penetrating injury
b) Blunt trauma
c) Orbital fracture
d) Chemical injury
Key Objectives
• Identify or exclude serious causes requiring immediate hospitalisation,
prompt referral and aggressive treatment.
• For conjunctivitis, define type to determine specific therapy.
Differentiate causal conditions that require prompt referral from those
that are less urgent.
processes of exclusion, differentiation, and diagnosis, viz :
History-taking essentials.
Skills for non-specialist examination of eye.
Selection and interpretation of appropriate investigations.
• Conduct an effective plan of management for eye redness:
Select patients in need of referral.
• Outline a management plan for the following causes of eye redness:
Conjunctivitis, foreign body, acute glaucoma.
173
036 Failure to Thrive
036A Infant/Child
Overview
Many infants and children do not follow the expected growth and development paths.
It is essential to differentiate the normal from the abnormal patterns.
Causes
11) Prenatal
a) Placental insufficiency
b) Antenatal infections
c) Prematurity
I 2) Perinatal
a) Acutely ill neonate- hypoxic ischaemia
13) Postnatal
a) Chronic disease
0 Cardiac, respiratory, gastrointestinal, neurologic, bone,
musculoskeletal
b) Poor intake
0 Maternal-infant bonding
0 Neglect
0 Environmental factors (famine)
c) Excessive utilisation
0 Acute or chronic infection
d) Malabsorption
0 Coeliac disease
0 Cystic fibrosis
0 Inflammatory bowel disease (IBD)
0 Malabsorptive enteropathies
Key Objectives
• Identify by comparing to normal growth charts the normal from the
abnormally growing and developing child.
• Identify the factors which will give rise to a chi ld who fails to thrive.
174
Plot growth parameters for any child at regular intervals so as to identify
any significant deviation from normal growth curve.
Obtain those features on history and physical examination known to be
associated with failure to thrive.
Diagnose the common causes of failure to thrive at the different age
groups.
Identify the various social risk factors responsible for failure to thrive.
Interpret growth parameters to diagnose failure to thrive.
Investigate with minimum but appropriate evaluations the commonly
associated problems associated with a child who is failing to thrive.
• Conduct an effective plan of management for a child/infant with a failure to
thrive:
Conduct a counselling and education programme for caregivers of
children with failure to thrive.
Conduct an ongoing programme to monitor the progress of such
children.
Appropriately utilise hospitalisation, consultation with other health
professionals and community resources.
Explain the social and psychological impact of failure to thrive on the
family and child.
175
036 Failure to Thrive
0368 Failure to Thrive in the Elderly
Overview
In an elderly person failure to thrive means the loss of energy, interest and vigour, with
or without weight loss. The challenge is to differentiate normal decline of strength with
ageing from reversible conditions which may be due to organic disease, environmental
factors or psychiatric disorders. Symptoms of serious organic disease are often minimal
or even absent in the elderly. Iatrogenic conditions also occur more often in the elderly
due to polypharmacy and resultant confusional states. Psychiatric disorders may
accompany or be secondary to organic disease, so the search for organic disorders
must be thorough before attributing decline to the ageing process or to environmental
causes. If clinical assessment does not reveal a cause the most productive
investigations in most cases are those which can be attained wi tho ut invasive
procedures.
Causes
1) Organic
a) Gastrointestinal (poor mastication/swallowing, malabsorption)
b) Cardiac/Respiratory disease
c) Metabolic (renal failure, diabetes)
d) Occult infections (especially urinary tract)
e) Malignancy- undiagnosed/advanced
f) Hyper/hypothyroidism
I2) Extrinsic I Functional 1 Social

a) Medications - especially adverse effects of polypharmacy
b) Inadequate diet
c) Loneliness and bereavement
d) Poverty and isolation (poor mobility)
e) Elderly abuse or neglect
f) Alcoholism
I 3) Psychiatric
a) Endogenous depression
b) Confusional states secondary to organic disease including vitamin
8 12 deficiency
c) Dementia
176
Key Objectives
• Select the investigations which screen the patient for occult organic
causes.
• Conduct an assessment of cognitive function using the Folstein Mini-
Mental State Examination (MMSE).
• Calculate the body-mass index (BMI) (=weight (kg)/height (M2 )) ; recognise
that figures outside 22-27 constitute a health risk.
Conduct a review of all body systems.
Check the status and management of known continuing health
problems.
Elicit information about the patient's environment and relationships.
• Interpret critical clinical and laboratory findings which are key in the process
Select further investigations or specialised care when indicated.
• Conduct an effective plan of management for an elderly patient who is
failing to thrive:
Treat the identified cause with specific therapy when possible.
Counsel the patient and relatives about cause , management and
prognosis.
List the support services which will improve isolation, nutrition, personal
care, medication use, independence and home care.
177
037 Falls
Overview
Falls are common (30% of people over 65 years; 50% by 80 years) and are associated
with functional disability, but they may be preventable. Interventions that prevent falls
and their sequelae may delay or reduce the frequency of nursing home admissions.
Causes
1) Factors extrinsic to the patient
a) Accidental and environmental factors
b) Medications/Alcohol
I2) Factors intrinsic to the patient

a) Age-related changes (e.g. vision , musculoskeletal, cortical function , etc.)
b) Syncope
(see #1 09 Syncope I Pre-Syncope I Loss of Consciousness)
c) DizzinessNertigo
(see #029 DizzinessNertigo)
d) Gait disturbances I Ataxia (
see #042 Gait Disturbances -Ataxia)
3) Other- narcolepsy, cryptogenic, depression
Key Objectives
• In a patient with one or more falls, elicit a description of the fall (obtain
collateral information if necessary) and conduct an evaluation of the
environment for risk factors.
• Differentiate between causes of falls by determining whether the fall was
secondary to factors intrinsic or extrinsic to the patient.
• Appreciate that a minority of falls are caused by a single, specific cause ;
the remainder are caused by more than a single factor.
Determine whether factors extrinsic to the patient may have caused the
fall (drugs, alcohol, environmental hazards such as poor illumination,
stairs, clutter, uneven or slippery surface, inappropriate footwear) .
Determine whether factors intrinsic to the patient may have caused the
fall (ataxia, cognitive impairment, impaired vision , gait disturbance,
other disease entities).
178
Conduct a physical examination and performance evaluation including
postural changes in blood pressure (BP), visual acuity, musculoskeletal
and neurological function , and footwear. Assess gait and balance.
Conduct an environmental assessment for hazards.
• Conduct an effective plan of management for a patient who has a tendency
to fall :
Counsel and educate the patient or caregiver about the complications,
morbidity, and mortality associated with falls. Describe the sequelae of
falls (injury, functional decline, restraints, immobility, death).
Treat correctable conditions.
Outline a management programme that includes control of risk factors
and provision of an active rehabilitation programme that focuses on gait
and balance retraining for seniors, with the provision of spectacles and
walking aids if appropriate.
List possible modifications in the living environment that reduce the risk
of falling (e.g. grab rails, sturdy furniture , improved lighting).
178
038 Fatigue
Overview
'Fatigue' means weariness from exertion but is used by both patients and doctors
synonymously with such terms as tiredness, weariness , lacking energy, listlessness,
sleepiness, exhaustion, weakness and being 'run down'. Possible causes are legion,
as indicated below.
Accordingly the symptom is not of high diagnostic value unless it is the outstanding
feature of a patient's presenting complaint or associated with certain other symptoms
such as loss of weight, chest pain, breathlessness, diarrhoea, rectal bleeding. An
organic cause will be found in only about one-third of patients with 'fatigue' as their
main complaint; many people with heavy domestic or occupational commitments present
- not unreasonably - with fatigue.
Of the remainder, about two-thirds will be suffering from a psychological condition.
Patients commonly use fatigue to somatise an underlying psychological problem. The
challenges are to identify underlying organic causes or associated pathology and
manage these appropriately, whilst recognising those patients without physical illness
who require more than simple reassurance and advice.
Causes
1) Psychologic
a) Depression
b) Anxiety
c) Somatisation
d) Bereavement
e) Lifestyle factors
I 2) Pharmacologic
a) Hypnotics
b) Antihypertensives
c) Antidepressants
d) Alcohol
e) Drug abuse or withdrawal
I 3) Endocrine/Metabolic
a) Hypothyroidism
b) Diabetes mellitus
c) Adrenal disease (Addison disease, Cushing disease)
d) Chronic renal failure
e) Chronic liver failure
f) Hypercalcaemia
g) Hypokalaemia
h) Hypomagnesaemia
180
I 4) Cardio-pulmonary
a) Chronic congestive heart failure
b) lschaemic heart disease
I 5) Infectious
a) Bacterial endocarditis
b) Tuberculosis (TB) and other chronic infections
c) Viral (mononucleosis, hepatitis, HIV, cytomegalovirus (CMV),
influenza)
I 6) Connective tissue disorders I

a) Rheumatoid arthritis (RA) I Polymyalgia
I 7) Sleep disturbances
a) Sleep-apnoea
b) Oesophageal reflux
c) Chronic pain interfering with sleep
I 8) Neoplastic-haematologic
a) Occult malignancy
b) Anaemia
I 9) Neuromuscular
a) Parkinson disease
b) Multiple sclerosis
c) Motor neurone disease
d) Myasthenia gravis
10) Idiopathic
a) Idiopathic chronic fatigue
b) 'Chronic fatigue syndrome'
c) ' Fibromyalgia '
181
Key Objectives
• Identify underlying organic disease if present.
• For patients whose fatigue does not have an organic basis, determine the
cause and provide advice about lifestyle, relationships or environmental
changes .
• Select patients who require more formal psychiatric treatment.
• Take a comprehensive history which includes details of presenting
symptoms. past history, family history, social and work history, habits,
systems review and current medication.
• Conduct a thorough physical examination, even when finding an
abnormality seems improbable.
• Use discrimination in the selection of investigations:
Directed at occult organic disease (e.g. anaemia, primary
hyperparathyroidism).
To followup diagnostic clues found in the history or physical
examination.
Be familiar with the criteria for the diagnosis of chronic fatigue
syndrome.
182
039 Fetal Distress J Non-Reassuring Fetal Status
Overview
Non-reassuring fetal status occurs in 5- 10% of pregnancies. Fetal distress, a term
also used for this situation, is imprecise and has a low positive predictive value. Thus,
when there is concern about fetal status, the newer term should be used.
Causes
1) Utero-placental insufficiency
a) Placental oedema (diabetes, hydrops)
b) Placental 'accidents' (abruption, praevia and/or accreta)
c) Post-dates
d) Intra-uterine growth restriction
j 2) Umbilical cord compression I

a) Umbilical cord accidents (prolapse, knot, anomalous insertion of
cord)
b) Oligohydramnios
13) Fetal conditions/anomalies

a) Sepsis (maternal, fetal, chorioamnionitis)
b) Fetal congenital anomalies
c) Prematurity
Key Objective
• Interpret information such as fetal heart rate and acid-base status after
considering patient's antepartum information and known risk factors in
order to identify non-reassuring fetal status.
183
• Through efficient focused data gathering:
Identify historical (e.g. hypertension, smoking) and examination risk
factors (e.g. fetal size less than expected).
List indications for fetal monitoring (antepartum and intrapartum).
Diagnose fetal tachycardia (greater than 160 bpm for more than
10 minutes) and fetal bradycardia (fewer than 120 bpm for more than
10 minutes), deceleration patterns, problems of short term variability,
reactivity.
Describe the measurement of fetal acid-base status (scalp pH , cord pH)
and list indications for such assessments.
• Conduct an effective plan of management for a patient whose fetus is in a
non-reassuring state:
Outline the management of post-term pregnancy.
Outline the management of infectious diseases during pregnancy that
may impair fetal development.
List causes of intra-uterine growth restriction .
List options regarding mode of delivery if fetal condition is possibly non-
reassuring.
While awaiting delivery, outline conservative measures for the
management of the mother (e.g. discontinue oxytocin, administer
oxygen to the mother, check maternal blood pressure (BP) and treat if
necessary, change maternal position to left lateral, volume expansion if
problem follows insertion of epidural).
Identify the short and long term consequences of fetal non-reassuring
status.
List risk factors for fetal congenital abnormalities (e.g. chromosomal ,
associated with teratogens).
Counsel parents with psycho-emotional consequences of fetal
development problems.
Select patients with non-reassuring fetal status for referral since in-
depth training and experience in obstetrics are required to manage the
condition adequately.
184
040 Fever and Chills (Adult and Paediatric)
Overview
Fever in children is the most common symptom for which parents seek medical advice.
Whi le most causes are self-limited viral infections (febrile illness of short duration) , it is
important to identify serious underlying disease and/or those other infections amenable
to treatment.
Causes
1) Febrile illness of short duration (less than two weeks)
a) Viral
0 With rash (varicella, morbilli, rubella, erythema infectiosum, roseola
infantum, Ross River fever, herpes simplex, herpes zoster)
0 Without rash (common cold, adenoviral, enteroviral, mumps, Epstein-
Barr virus (EBV), cytomegalovirus (CMV), influenza, hepatitis A,
Murray Valley encephalitis)
b) Bacterial
I.J With rash (meningitis, scarlet fever, impetigo)
U Without rash (streptoccocal pharyngitis, pneumon ia, urinary,
meningitis, skin)
c) Other infectious agents (mycoplasma pneumonia)
2) Prolonged febrile illness (more than two to three weeks)

(see #040A Fever/Pyrexia of Unknown Origin (PUO))
a) Familial-hereditary diseases
b) Other (malaria, tuberculosis (TB), Hodgkin lymphoma)
Key Objectives
• Determine whether the febrile illness is of short duration or is prolonged.
• Differentiate between acute viral or pyogenic infections, and contrast to
prolonged febrile illness.
185
Differentiate infectious from noninfectious causes of fever.
Identify the common causes and risk factors of fever in the various age
groups.
Use relevant and cost-effective measures to investigate causes of fever
and exclude more serious problems.
• Conduct an effective plan of management for a patient with fever:
Outline the management of a septic child and initiate immediate
resuscitation measures if necessary.
Outline the management of a specific febrile illness.
Select patients in need of referral or specialised care.
Perform specific technical procedures to diagnose the cause of fever.
Counsel parents, family, or caregivers about the care of children with
febrile illnesses.
Discuss use of aspirin in children with acute febri le illness and influenza
vaccination complications.
Discuss the relevant features of pandemic, epidemic, and endemic
influenza, populations at highest risk of infection and/or complications of
influenza, and measures taken to modify the illness and prevent the
predictable excess mortality of influenza.
186
040A Fever/Pyrexia of Unknown Origin (PUO}
Overview
Fever/Pyrexia of unknown origin (PUO) defines a febrile illness of three weeks or more
without an established diagnosis despite extensive investigation.
Causes
1) Infections (approximately one-third of cases)
a) Systemic
0 Endocarditis
0 Tuberculosis (TB)
0 Malaria
0 Other infections (e.g. brucellosis, Q fever)
b) Localised
0 Abscess
• Contiguous spread (e.g. liver, sub-phrenic from hepato-biliary,
bowel)
• Haematogenous spread (e.g. splenic)
• Perinephric/Renal
0 Osteomyelitis
0 Central nervous system (CNS) infections (meningitis, encephalitis)
Osler nodes
1 87
2) Neoplasms (approximately one-third of cases)
a) Lymphoma/Leukaemia
b) Solid (renal cell, hepatoma/metastases)
I3) Multi-system
a) Collagen disease (systemic lupus erythematosus (SLE), rheumatoid
arthritis (RA))
b) Granulomatous (sarcoidosis, giant cell arteritis, other vasculitis)
c) Drug reactions
d) Miscellaneous (e.g. factitious)
Key Objectives
• Perform repeated clinical assessments searching for unusual presentations
of common conditions.
• Elicit a history of travel, animal exposure, whether the patient may be
immunosuppressed, is taking any type of medications (e.g. antimicrobial
drugs) or had contact with toxins.
Perform a detailed history and physical examination, especially
searching for localising symptoms and signs.
Conduct the minimum diagnostic investigation based on causal
conditions most frequently associated with fever of unknown origin.
List indications for lumbar puncture, computed tomography (CT) scan of
head or spine, serologic testing, or biopsy.
• Conduct an effective plan of management for a patient with fever of
unknown origin:
State reasons why therapeutic trials without a firm diagnosis are
generally counterproductive.
Outline a management plan consistent with the underlying causes.
188
0408 Fever in the Immune-Compromised Host I

Recurrent Fever
Overview
Patients with certain immunodeficiencies are at high risk for infections, the infective
organism and site depending on type and severity of immuno-suppression. Some of
these infections are life-threater ·
1) Defects in cell-mediated immunity (T cells)

a) Acquired cell-mediated immunity defect (HIV/AIDS, Hodgkin disease,
immuno-suppressive therapy, lymphocytic leukaemia)
b) Inherited cell-mediated immunity defect
2) Defects in humoral immunity (B cells)

a) Loss (e.g. nephrotic syndrome)
b) Decreased production (in infancy, transient; myeloma, lympho-
proliferative disease)
3) Complement deficiencies (collagen disease, not necessarily

associated with infection)
4) Asplenia (splenectomy, congenital absence, sickle cell disease,

systemic lupus erythematosus (SLE), etc.)
5) Neutrophil dysfunction (granulomatous disease, uraemia,

cirrhosis)
RsshofSLE
189
j 6) Neutropenia
(see #01 0 Abnormalities of White Blood Cells)
7) Anatomic barriers abnormal (surgery, foreign bodies, burns,

desquamating rash)
Key Objectives
• Determine if patients with fever have isolated febrile episodes or recurrent
ones, single or multiple anatomic sites involved in infections, past history of
infections and infections in relatives.
• Determine whether possible exposure to HIV occurred.
• Determine if immuno-suppressive or anti-infective medications are being
taken or have recently been administered.
Determine whether it is likely the patient with fever is immune-
compromised (e.g. persistent lymphadenopathy).
Determine whether the site of infection is single or multiple, and which
body systems are likely to be involved (e.g. upper respiratory tract,
lungs, skin, gastro-intestinal tract, nervous system).
Determine, if possible, the type of infection and/or organism isolated in
previous infections.
Select serum protein electrophoresis in a patient suspected of
hypogammaglobulinaemia.
Select sites from which cultures should be obtained and interpret
results .
Investigate a patient suspected to have HIV (HIV serology).
Select appropriate diagnostic imaging.
Contrast the type of organisms likely to cause infection in patients with
asplenia or hypogammaglobulinaemia compared to organisms in cell-
mediated immune defect.
• Conduct an effective plan of management for an immune-compromised
patient with fever:
Outline the initial management of a febrile patient who is immune-
compromised .
Discuss indications for intravenous (IV) gamma globulin replacement
therapy.
Discuss indications for prophylactic pneumococcal vaccination .
190
040C Fever in the Neonate (in Child Less than

Four Weeks}
Overview
Fever in neonates is serious, and the cause must be immediately identified and treated.
Causes
11) Infections
a) Bacterial
0 Pneumonia
0 Urinary tract
0 Septicaemia
Meningitis
Omphalitis
0 Osteomyelitis, septic arthritis
0 Conjunctivitis
b) Toxoplasmosis
c) Viral
Cytomegalovirus (CMV)
Herpes
0 Rubella
0 Other
j2) Overheati ng (e.g. in isolette ) I

Key Objective
• Rapidly assess the neonate to establish a working diagnosis and institute
treatment immediately.
Identify the features of a septic neonate.
Recognise that fever may be absent in a neonate with sepsis.
Identify the risk factors for sepsis in the neonate including maternal,
host, immunologic and environmental factors.
Identify the causes of fever in the neonate.
191
Outline relevant and cost-effective investigations for a neonate with
fever.
Contrast the differences in laboratory features in neonates and older
infants and children with sepsis.
• Conduct an effective plan of management for a fever in the neonate:
Outline resuscitative measures in neonates with sepsis.
Outline the management of specific causes of sepsis in the neonate.
Perform specific procedures to diagnose cause of neonatal fever.
Counsel parents regarding the important issues in the short and long
term outcome of neonatal fever.
192
040D Hypothermia
Overview
Although far less common than is elevation in temperature, hypothermia (central
temperature less than 35°C) is of considerable importance because it can represent a
medical emergency.
Causes
1) Accidental/Immersion hypothermia (exposure to cold)
2) Hypothermia with acute illness (associated with metabolic

acidosis, cardiac arrhythmias)
a) Decreased heat production (hypothyroidism, drug overdose,
diabetes mellitus, hypoglycaemia, congestive heart failure)
b) Increased heat loss (cirrhosis, uraemia, respiratory failure, drug
overdose)
c) Impaired thermoregulation (stroke, drug overdose)
Key Objective
• State that hypothermia is a potential medical emergency and urgent
therapy may be necessary.
193
• Conduct an effective plan of management for a patient with hypothermia:
Outline an emergency management plan.
Contrast the advantages and disadvantages of active external re-
warming and active core re-warming in accidental hypothermia.
In patients with hypothermia secondary to acute illness, determine
whether alcohol or other drugs were ingested.
Determine whether previous illnesses may have precipitated the
hypothermia.
Select, list, and interpret investigations immediately after therapy is
initiated.
Recognise and prevent the potential hazards of iatrogenic hypothermia
(massive transfusion, prolonged surgery, etc.).
194
040E Hyperthermia
Overview
Hyperthermia is an elevation in core body temperature due to failure in thermo-regulation
(in contrast to fever, which is induced by cytokine activation). Although the differential
diagnosis is extensive (includes all causes of fever) , the three conditions listed below
may be associated with severe complications and death.
Causes
1) Heat stroke
a) Classic
b) Exertional
2) Neuroleptic malignant syndrome (NMS)
I 3) Malignant hyperthermia
Key Objective
• Determine the context in which the symptoms developed (e.g. malignant
hyperthermia after anaesthetic, NMS after antipsychotics).
Elicit a history of chronic medical conditions that either impair
thermoregulation or prevent removal from a hot environment, heavy
exercise in high ambient temperatures, anaesthetics, or antipsychotics.
Perform examination including rectal temperature, presence of
pulmonary oedema, cardiac examination, evidence of bleeding, central
nervous system (CNS) dysfunction, muscle tone.
115
• Interpret critical clinical and laboratory findi ngs which were key in the
Select investigations for the determination of disseminated intravascular
coagulation (DIG), rhabdomyolysis, renal or hepatic fai lure, arrhythmias,
pulmonary oedema.
• Conduct an effective plan of management for a patient with severe
hyperthermia:
Recognise that external cooling may be potentially detrimental.
Outline various methods of cooling a hyperthermic patient, and indicate
when to stop the cooling process.
Outline initial management.
198
041 Fractures I Dislocations
(See also # 113 Trauma/ Accidents/Prevention and # 1138 Bone and Joint
Injuries)
Overview
Fractures and dislocations are common problems at any age and are related to high-
energy injuries (e.g. motor accidents, sport injuries) or, at the other end of the spectrum,
simple injuries such as falls (see #037 Falls). Fractures and dislocations in children
and young adults tend to be due to motor vehicle and sports injuries whereas in the
elderly the cause is more likely to be associated with relatively minor trauma such as a
fall.
Dislocated shoulder - axillary Supracondylar humeral

nerve at risk fracture - brachial artery at risk
Causes
11) Fractures - traumatic
I 2) Fractures - pathologic
a) Metabolic bone disease
b) Tumours (benign, malignant, primary, secondary)
I 3) Fractures - stress
4) Dislocations and fracture/dislocations
Key Objectives
• In traumatic fractures recognise the importance of differentiating 'open' from
'closed' injuries and the need for early wound closure in the former.
• Appreciate and identify accurately and promptly the potential vascular and
neurologic complications of common fractures and dislocations.
197
Stress fracture tibia Pathological fracture femur
Determine limb function , local soft tissue changes (closed or open
fracture), bone or joint disruption, active and passive range of motion,
status of joint above and below suspected long bone fracture.
Determine neurologic and vascular status distal to level of injury.
If minimal trauma causes a fracture, elicit history of conditions
associated with pathologic fractures (metabolic bone disease, tumours) ,
or identify activity that involves highly repetitive low-level stress (e.g.
marching, running, ballet dancing).
Select skeletal elements to be included in the diagnostic imaging
required , as well as views.
List circumstances requiring additional diagnostic imaging such as
computed tomography (CT), imaging of opposite side for comparison ,
joint above and below, bone scan, etc.
Outline investigation plan in a patient with a pathologic bone fracture.
• Conduct an effective plan of management for a patient with fractures I
dislocations I joint injuries:
Recognise differing requirements for management of stable and
unstable fractures.
List methods to obtain and maintain appropriate reduction.
Determine whether closed or open treatment is required and select
patients requiring referral.
List complications of limb immobilisation and methods of maintaining
reduction (e.g. plaster cast).
Outline management of specific fractures (e.g. stress fracture,
pathological fracture) .
198
042 Gait Disturbances- Ataxia
Overview
Abnormalities of gait can result from disorders affecting several levels of the nervous
system and the type of abnormality observed clinically often indicates the site affected.
Causes
1) Disorders of balance
a) Cerebellar ataxia - midline lesions (tumours, haemorrhage, infarct,
multiple sclerosis, drugs, toxins)
b) Sensory ataxia
0 Vestibular
(see #029 DizzinessNertigo)
0 Proprioceptive
(see #069 Numbness and Tingling)
0 Visual
(see #120 Visual Disturbance/Loss)
I 2) Disorders of locomotion
a) Weakness disorders
(see #122 Weakness/Paralysis/Paresis)
b) Parkinsonian gait
(see #057 Involuntary Movement Disorders I Tic Disorders)
c) Higher level gait disorders (disorders of frontal lobes, basal ganglia,
thalamus, midbrain such as stroke, hydrocephalus, dementia,
tumours)
d) Antalgic gait (disorders of the musculoskeletal system such as
degenerative joint diseases and other arthropathies, deformities of
legs, spinal disorders)
I3) Hysterical gait
Key Objective
• Determine whether the gait disturbance occurs more in the dark or light
(sensory), whether giddiness or vertigo (vestibular) accompanies the
disturbance, presence or absence and distribution of muscle weakness,
and whether there is pain, numbness, or tingl ing in the limbs (sensory).
199
Differentiate between cerebellar and sensory ataxia.
Determine whether there is weakness (difficulty rising from a chair,
fatiguability of muscles), stiffness, or pain (trauma to legs, pelvis or
spine, arthritis).
Outline initial investigation for a patient with an abnormal gait.
Select patients in need of referral for further investigation.
• Conduct an effective plan of management for a patient with gait
disturbance/ataxia:
Outline a management plan for patients with antalgic gait.
2 00
043 Genetic Concerns, Dysmorphic Features
(See also #129A Congenital Malformations)
Overview
Three out of 100 infants are born with a congenital defect or genetic disorder. Many of
these are associated with a mental retardation or learning disability. Although early
involvement of genetic specialists in the care of children with dysmorphic disorders is
prudent, primary care clinicians are at times, required to contribute immediate care,
and subsequently, assist with long term management of such patients.
Causes
1) Teratogenic disorders (fetal alcohol syndrome, cocaine,
coumarin)
12) Chromosomal disorders

a) Down syndrome
b) Turner syndrome
c) Fragile X chromosome
d) Klinefelter syndrome
13) Genetic syndromes

a) Tuberous sclerosis
b) Neurofibromatosis
c) Duchenne muscular
dystrophy
Congenital ear malformation Sturge-Weber syndrome
201
Key Objective
• Demonstrate empathy for parents' concern , if diagnosis is known , outline
probable course/management, and discuss early referral for specialised
care , if appropriate.
Formulate a phenotype from relevant family history.
Determine exposure, if any, to teratogens in pregnancy.
Differentiate chromosome disorders or genetic syndromes in the family
from other types of dysmorphic features .
List indications for antenatal screening in a subsequent pregnancy.
Determine by seeking the advice of a specialist whether any immediate
investigation is required prior to referral.
• Conduct an effective plan of management for a patient with dysmorphic
features :
Explain the alternatives for dealing with the risk of recurrence.
Counsel families or refer for genetic counselling if a genetic disorder is
identified concerning future risks and prenatal strategies for the
prevention of dysmorphic disorders.
Discuss with the parents that the long term care will depend on the
diagnosis and prognosis, but may involve specialised medical care,
multidisciplinary services, family support, and if necessary, academic
support and child placement.
Conjoined twins
202
043 Genetic Concerns, Dysmorphic Features
043A Genetic Concerns, Screening
Overview
Advances in genetics have increased our understanding of the origin of many diseases.
Not infrequently, spouses who are considering becoming parents, or have just conceived,
seek medical advice because of concerns they might have. Primary care clinicians
and others must provide counselling and referral if further evaluation is necessary.
Causes
11) Chromosome defects
a) Numerical (Down syndrome)
b) Structural (cri-du-chaf)
2) Mendelian - common causes are listed below

a) Dominant
0 Huntington chorea
0 Familial hypercholesterolaemia
0 Polycystic kidney disease
b) Recessive (cystic fibrosis)
c) X-linked
0 Haemophilia
0 Duchenne muscular dystrophy
3) Multifactorial conditions (neural tube defects)
Key Objective
• Elicit history on the proband or index case (the clinically affected person
who has brought the family to the attention of the clinician) and of each of
the first-degree relatives (parents, siblings, and offspring of the proband).
Formulate a three-generation pedigree.
203
Elicit history regarding prior obstetrical, medical, and family history,
exposure or concerns during current pregnancy, age of mother at date
of delivery.
Determine whether there are relatives with identical , similar, or
associated features, or a problem recognised to be genetically
determined: is there consanguinity, what is the ethnic origin of the
family? Unexplained early neonatal death may indicate an inherited
genetic disorder.
Identify/search literature for physical characteristics/hallmark features of
genetic conditions.
List diagnostic tests available for prenatal diagnosis in a subsequent
pregnancy (e.g. amniocentesis, fetal blood sampling); discuss
sensitivity, specificity, expense, and risk of such testing.
Differentiate between screening tests and diagnostic tests for
chromosome disorders and list indications.
Select patients who require consultation with a DNA laboratory or
geneticist consultant regarding additional investigation and plan this
prior to next pregnancy.
• Conduct an effective plan of management for screening genetic concerns/
dysmorphic features:
Counsel pertinent family members by explaining meiosis, mitosis, and
errors leading to aneuploidy.
Select patients for referral to genetics specialists, community resources,
social support groups, etc.
Counsel patients regarding alternative reproductive options (e.g.
contraception, therapeutic donor insemination, donor ova, adoption,
prenatal diagnosis with/without therapeutic termination of affected fetus,
embryo biopsy and assessment within an invitro-ferti lisation programme
(IVF) (with subsequent transfer of normal embryos only).
204
044 Hair and Nail Disorders
044A Hair Disorders
Overview
Symptoms of too little or too much hair are common. Loss of hair and hirsutism may
have serious effects on self-esteem. A correct diagnosis is usually possible from
systematic history-taking and examination. Hair changes can provide significant hints
of underlying systemic disease. A treatable underlying cause may be present; but
treatment is poorly effective except when an accompanying local inflammatory disorder
is present.
Causes
1) Alopecia (hair loss)
a) Primary
0 Alopecia areata, alopecia totalis, alopecia universalis
(poor prognosis)
0 Acute telogen effluvium - pregnancy, surgery, acute illness etc.
(good prognosis)
b) Secondary
f.J Chronic telogen effluvium
• Metabolic and endocrine disorders (thyroid, diabetes, puberty)
• Iron and zinc deficiency
• Advanced malignancy
• Malnutrition
0 Anagen effluvium
• Chemotherapy and radiation therapy
• Poisoning (thallium, mercury, arsenic)
0 Androgenic alopecia
• Male pattern baldness
• Female pattern baldness
0 Infections (tinea capitis)
Alopecia areata
205
Alopecia tots/Is
2) Hirsutism
(see #052 Hirsutism and Virilisation)
a) Virilisation absent
0 Idiopathic
0 Familial
Drugs (minoxidil, cyclosporine, phenytoin)
b) Virilisation present (clitoromegaly, male habitus, voice deepening)
Androgenic excess from ovarian or adrenal source
3) Local inflammation
a) Scaly scalp disorders
0 Dandruff (pityriasis capitis)
0 Seborrhoeic dermatitis
0 Psoriasis
b) Infective hair disorders
0 Folliculitis barbae
Tinea capitis
Lice (pediculosis)- head, pubic
Tines capitis
206
Key Objectives
• In patients with alopecia:
Identify type of hair loss.
Exclude secondary causes and establish whether scarring is present.
• In patients with hirsutism:
Determine whether viril isation is present, indicating need for full
investigation.
Differentiate between various causes by seeking corroborative
evidence.
• Interpret critical clinical and laboratory findings wh ich were key in the
• Interpret influences of hair cycles of anagen (the growing phase) and
telogen (the resting phase when hair is normally shed).
• Conduct an effective plan of diagnosis and management for a patient with
alopecia.
• Conduct an effective plan of diagnosis and management for a patient with
other local hair disorders.
207
044 Hair and Nail Disorders
0448 Nail Disorders
Overview
Nail changes frequently provide significant hints of underlying systemic disease.
Changes in colour, surface or shape may be diagnostic.
Local medical and surgical nail disorders may involve nail bed and germinal matrix,
nail plate, nail fold sulcus, lateral nail fold , or cuticle.
Causes
1) Nail changes in systemic disease
Nail sign Condition
a) Colour change
0 Nail bed pallor Anaemia
0 Blue nails Cyanosis, Wi lson disease
0 Red nails Polycythaemia, carbon
monoxide poisoning
0 Yellow nails Jaundice, tinea, tetracycline,
yellow nail syndrome
0 Brown nails Nicotine, psoriasis, poisons
0 White nails - leuconychia Hypoalbuminaemia
('liver nails')
0 Black nails Haematoma, melanoma
0 Splinter haemorrhages Infective endocarditis,
vasculitis, subclavian artery
compression, blood
dyscrasias, trauma
Nails In liver dlse8sll Pitted nails - psoriasis
208
b) Surface change
0 Transverse grooves (Beau lines) Serious illness or local trauma
0 Opaque white transverse bands As above, also
(Muehrcke or Mees lines) hypoalbuminaemia, poisons,
chemotherapy
0 Pitting Psoriasis, chronic paronychia
0 'Half and half' nails (white Chronic renal disease,
proximal and red distal) cirrhosis
c) Shape change
0 Clubbing Lung cancer, chronic lung
suppuration, cyanotic heart
disease, infective endocarditis,
ulcerative colitis, thyroid
acropathy in Graves disease
0 Spoon shaped (koi lonychia) Iron deficiency anaemia,
diabetes
0 Onycholysis (separation of Thyrotoxicosis, psoriasis,
nail plate from nail bed) trauma
0 Nail fold erythema Systemic lupus erythematosus
and telangiectasis (SLE), and other connective
tissue disorders
0 Hypoplastic Congenital syndromes
0 Onychogryposis (ram-horn nail) Trauma, fu ngal infection,
ischaemic, idiopathic
Grooved nail- mucous cyst of ns/1 bed
209
I 2) Other local nail disorders
a) 'Hang nail' - cuticle tear
b) Nail-biting- habit associated with emotional concerns
c) Chipped, engrimed - manual labouring occupations
d) Paronychia ('whitlow') infected nail fold, acute or chronic, bacterial,
fungal, herpetic (dishwashers, diabetics and nurses)
e) Onychomycosis - tinea unguim, more frequent in toenails
f) Ingrown toenail - onychocryptosis
g) Mucous cyst of nail bed I nail fold
h) Subungual haematoma or melanoma
i) Glomus tumour- marked tenderness
j) Hereditary pachyonychia
k) Drug effects - minocycline, tetracycline, antimalarials, retinoids,
nicotine staining
Key Objectives
• Make nail assessment an integral component of examination of the limbs.
• Differentiate between changes in colour, surface and shape.
• Be alert to nail changes in systemic disease.
Differentiate between various causes by seeking corroborative
evidence.
• Conduct an effective plan of management for a patient with a nail disorder.
• Select patients in need of referral.
Ram-hom nail- onychogryposis Subungual haematoma
210
045 Head Injuries I Brain Death I Transplant Donation
Overview
Most head injuries follow blunt trauma. Fractures of the skull can be open/compound
externally in association with scalp wounds, or internally from basal fractures. Cerebral
concussion, contusion and laceration represent a spectrum of increasingly severe
primary damage. The most important aspect of clinical neurological assessment is
level of consciousness, together with abnormal neurological signs. Cerebral
compression with progressive clinical deterioration is seen in patients with complications
resulting from haematoma formation, cerebral oedema or hypoxic damage. A computed
tomography (CT) scan is an essential baseline investigation in the patient with a severe
head injury.
Causes
1) Blunt or penetrating injuries with or without skull fracture
2) Cerebral concussion, contusion, laceration
3) Cerebral haemorrhage/haematoma (epidural, subdural,

subarachnoid, intracerebral)
14) Cerebral oedema/compression
Epidural haematoma
Depressed skull fracture
Key Objectives
• Grade level of consciousness on Glasgow Coma Scale using responses of
eye opening, best motor response and best verbal response.
• Select CT scan of the head in a patient, whose mental status is depressed
or worsening , has focal neurologic deficit, depressed skull fracture, or
penetrating head injury.
211
Elicit history on more than one occasion to detect change in mental
status.
Perform neurological examination on more than one occasion.
Contrast time course for appearance of abnormal findings on head CT
for epidural haematoma from middle meningeal artery injury from
epidural or subdural haematoma resulting from venous injury.
Order repeat head CT for patient whose neurologic condition
deteriorates or fails to improve as expected.
• Conduct an effective plan of management for a patient with head injury:
Assess patients with deep non-responsive coma for criteria of brain
death by establishing diagnosis of irreversible absence of brain stem
reflexes and permanent absence of spontaneous breathing under
conditions that exclude the effects of hypocapnia and neuromuscular
blocking drugs.
In a patient whose head injury has caused brain death but the heart is
beating, communicate this information to the transplantation team (or
equivalent) if the deceased patient or the family have indicated a desire
to donate organ(s).
If there is no indication that organ donation has been considered ,
counsel, with empathy, the family regarding the possibility.
Subdural haematoms
212
046 Headache
Overview
The differentiation of patients with headaches due to serious or life-threatening conditions
from those with benign primary disorders (e.g. tension headaches or migraines) is an
important diagnostic challenge. Contrary to popular belief, 'eye strain' is not a com mon
cause of headache.
Causes
1) Migraine
a) With aura
b) Without aura
2) Tension-type headache (also headache with

medication overuse)
I 3) Cluster headache
4) Headache associated with

vascular disorders
a) Subarachnoid haemorrhage
b) Temporal arteritis
c) Venous thrombosis
d) Intracranial haematoma (including
epidural, subdural)
e) Severe arterial hypertension Anterior cerebral artety
BIJ8Urystn
5) Headache associated with nonvascular
intracranial disorder
a) Elevated cerebrospinal fluid (CSF)
pressure (intracranial mass lesion or
hydrocephalus)
b) Intracranial infection (meningitis,
abscess, sinusitis)
I 6) Miscellaneous
a) Systemic viral infection
b) Psychological disorders
c) Medication use (nitroglycerin) or
medication withdrawal (analgesic)
Cerebral arteriovenous
d) Cervical spondylosis malformation
e) Poor working ergonomics (computer

screen at wrong level, etc.)
213
Meningioma
Key Objective
• Elicit the signs and symptoms that help distinguish potentially serious from
benign headaches.
Differentiate between the various causes of headaches.
Select patients in need of immediate management.
Outline and interpret appropriate and cost-effective laboratory and
diagnostic imaging tests used in the assessment of patients with
headaches.
• Conduct an effective plan of management for a patient with a headache:
List the indications and contraindications for the use of various
analgesic medications and for the prophylactic use of specific
medications.
Outline use of analgesics and ergotamine for the purpose of avoiding
the development of chronic daily headaches secondary to medication
overuse.
Provide patient education and counselling regarding the causes and
management of headaches.
Identify patients with complications related to narcotic therapy and
addiction.
214
047 Hearing Loss I Deafness
Overview
There are many causes for hearing loss, many treatable and/or preventable. In
paediatrics, otitis media accounts for 25% of all office visits. Although adults and older
children have otitis less commonly, they may be affected by otitis sequelae.
Causes
1) Conductive hearing loss
a) External ear pathology
0 Inflammation or infection
0 Obstruction of canal (wax, foreign body, tumour)
b) Middle ear pathology
0 Otitis media (acute, serous, chronic)
0 Cholesteatoma
0 Ossicular pathology (otosclerosis, fracture)
0 Tumours (glomus, adenoma)
2) Sensorineural hearing loss (sudden, chronic)

a) Cochlear (inner ear) pathology
0 Presbycusis of old-age
0 Loud noise
0 Ototoxic drugs (aminoglycosides)
0 Trauma (temporal bone fracture)
0 Inner ear disease (Meniere disease, autoimmune, etc.)
b) Retro-cochlear/central pathology
0 Cerebellopontine angle tumours (acoustic neuroma, meningioma)
0 Infection (meningitis)
0 Multiple sclerosis
0 Vascular occlusion
c) Congenital
o Hereditary, congenital syndromes
0 High-risk birth 'TORCH' infections ( Toxoplasmosis, Qther, Bubella,
Qytomegalovirus, Herpes simplex virus) , low birth weight, etc.
215
Key Objectives
• Differentiate between conductive and sensorineural hearing loss by history
and tuning fork test.
• Communicate primary prevention strategy (ear noise protection).
Elicit history mindful of the non-specific symptoms of otitis in younger
children; examine after wax removal ; identify risks of hearing loss
(familial, industrial, drugs, at birth).
Differentiate conductive and sensorineural hearing loss with a tuning
fork test.
Differentiate conductive and sensorineural hearing loss on audiograms.
• Conduct an effective plan of management for a patient with hearing loss I
deafness:
Outline a management and followup plan for a patient with otitis,
selecting appropriate antibiotics.
• Counsel and educate patients about primary prevention of hearing loss
(e.g. ear noise protection).
216
048 Haematemesis/Melaena
Overview
Haematemesis, although often self-limited, is likely to be large and severe in elderly
patients with arteriosclerotic vessels and may be associated with considerable mortality
and morbidity without urgent management. Mortality and morbidity is also high in
patients with portal hypertension.
Causes
1) Ulcerative/Erosive
0 Idiopathic
0 Drugs (nonsteroidal anti-inflammatory drugs (NSAIDs), corticosteroids,
immunosuppression)
Infectious (Helicobacter pylori, cytomegalovirus (CMV), herpes
simplex)
0 Stress ulcer (postoperative, post-trauma, intensive care patients)
b) Oesophagitis
0 Peptic
Infectious
Pill-induced, e.g. potassium chloride
I 2) Portal hypertension
3) Trauma I Severe vomiting (Mallory-Weiss syndrome)
4) Vascular malformations (angiomas, hereditary haemorrhagic

telangiectasia (Osler disease))
I 5) Tumours (benign, malignant)
Bleeding gastric ulcer
217
Key Objectives
• Determine the haemodynamic stability of the patient and the resuscitation
measures required.
• Select patients requiring admission to intensive care units.
• Select diagnostic studies after adequate resuscitation and stabilisation (to
prevent complications of endoscopy) and deliver associated treatment if
required .
Diagnose the likely cause of haematemesis.
Select appropriate investigations for the causes of haematemesis, and
determine whether bleeding disorders are present.
List the indications for diagnostic endoscopy and diagnostic imaging.
List findings suggesting that likelihood of re-bleeding is high.
• Conduct an effective plan of management for a patient with haematemesis:
Outline the mechanism of action of various medical treatments.
List indications for pharmacological, endoscopic or surgical treatment.
Outline subsequent treatment to decrease recurrence.
218
049 Haematuria
Overview
Haematuria is bleeding via the urinary tract and may be a dramatic presentation of
renal or urinary tract pathology (frank haematuria) or a condition that is only detected
on dipstick testing and/or microscopic examination. Phase contrast microscopy, except
in frank haematuria, can indicate whether the bleeding is more likely to be of kidney
origin (glomerular) or not.
Causes
11) Transient
a) Urinary tract infections (UTis)
b) Exercise-induced
c) Glomerulonephritis
d) Stones/Crystals
e) Trauma
f) Endometriosis
g) Thromboembolism
h) Anticoagulants
12) Persistent
a) Extraglomerular
0 Renal
• Tumours
• Tubulointerstitial diseases
(e.g. polycystic kidney
disease, pyelonephritis)
• Vascular (e.g. papillary
necrosis, sickle cell
disease)
0 Collecting system Renal cell tumour
• Tumours
• Stones
b) Glomerular
0 Isolated (e.g. immunoglobulin A (lgA) nephropathy, thin membrane
disease)
0 Post-infections (e.g. post-streptococcal)
0 Systemic involvement (e.g. vasculitis, systemic lupus erythematosus
(SLE))
219
Key Objective
• Differentiate red urine from haematuria, frank from microscopic haematuria,
transient from persistent haematuria, and glomerular from extraglomerular
haematuria.
Determine whether the patient has true haematuria.
Diagnose the presence of UTls.
Differentiate between glomerular and extraglomerular haematuria.
Interpret reported urinalysis findings.
Outline significance of patient's age, gender, and lifestyle on diagnostic
possibilities.
Formulate a diagnostic plan for a patient with frank haematuria.
• Conduct an effective plan of management for a patient with haematuria:
Select treatment for patients with UTis appropriate for gender, and for
lower and upper urinary tract.
Outline a plan for investigation of patients with recurrent nephrolithiasis.
Formulate a management plan for prevention of recurrent
nephrolithiasis.
Discuss possible strategies for the detection and prevention of urinary
tract tumours.
Large vesical calculus
220
050 Hemiplegia I Hemisensory Loss I Stroke with or
without Aphasia 1 Prevention of Stroke
Overview
Stroke is a focal neurologic deficit lasting longer than 24 hours, of presumed vascular
origin. If the deficit lasts less than 24 hours, it is termed transient ischaemia. These
arbitrary definitions are conventional but it is now recognised that a significant proportion
of patients with transient ischaemic attacks will have pathological lesions on cerebral
imaging (computed tomography {CT) and magnetic resonance imaging (MRI)). Vascular
causes of neu rological deficit usually have a sudden onset. Hemiplegia and
hemianaesthesia arise from a lesion above the mid-cervical region , and aphasia
indicates the involvement of the dominant cerebral hemisphere. The occurrence of a
stroke or transient ischaemia indicates significant vascular, cardiac or haematological
disease demanding investigation and appropriate medical or surgical treatment.
Causes
1) Stroke or transient ischaemia
a) lschaemic
0 Embolism, thrombosis, hypoperfusion
b) Cerebral haemorrhage
0 'Spontaneous'
0 Vascular malformation
0 Clotting disorder
c) Subarachnoid haemorrhage
0 Usually indicating intracerebral bleeding or vascular spasm
I 2) Postepileptic (Todd palsy)
I 3) Head trauma
a) Cerebral contusion with haemorrhage and oedema
b) Extradural haematoma
c) Subdural haematoma
4) Intracranial space-occupying lesions

a) Primary and secondary malignancy
b) Benign tumours
c) Cerebral abscess
I 5) Hemiplegic migraine
221
I 6) Demyelination
a) Encephalomyelitis
b) Multiple sclerosis
7) Infections
a) Encephalitis
b) Toxoplasmosis (in AIDS)
Key Objectives
• Recognise the risk factors for stroke within the community, and recommend
appropriate preventive measures.
• Diagnose the cause of hemiplegia, on the basis of history, cl inical findings
and neuro-imaging studies.
• Diagnose the cause of transient ischaemia and minor stroke and
recommend appropriate medical or surgical treatment to prevent further
stroke.
• Through efficient history-taking:
Differentiate between the causes of hemiplegia based on history, time
course, clinical findings and risk factors.
Identify transient ischaemic syndromes including transient monocular
blindness (amaurosis fugax) , transient hemispheric syndromes and
vertebrobasilar syndromes including visual, brainstem and cerebellar
symptoms.
• Interpret critical clinical findings , laboratory data and CT and MAl scan
images necessary to arrive at a presumptive diagnosis.
Recognise the CT scan appearance of large vessel and lacunar
cerebral infarction, cerebral haemorrhage, subarachnoid haemorrhage,
extradural haematoma, subdural haematoma, cerebral contusion and
intracranial space occupying lesion.
Recommend other appropriate laboratory and imaging studies
(including contrast CT and MAl) if requi red to arrive at a definitive
diagnosis.
• Recommend an immediate plan of investigation and treatment for all
patients presenting with transient ischaemia.
222
• Describe an effective plan of management for a patient with hemiplegia:
Outline the acute medical management of patients with ischaemic and
haemorrhagic strokes.
Discuss the primary and secondary preventive measures used in the
prevention of ischaemic stroke, including medications (anti-platelet and
anticoagulant) and carotid endarterectomy.
Outline the management in the prevention of stroke of a patient with
atrial fibrillation .
Understand the effective and timely use of rehabilitation.
223
050 Hemiplegia I Hemisensory Loss I Stroke with or
without Aphasia I Prevention of Stroke
050A Paraplegia/Paraparesis
Overview
Acute paraplegia should be identified as a medical emergency which may require urgent
surgery. Spinal cord lesions cause lower motor neuron signs at the level of the lesion
and upper motor neuron signs below that level. High cervical lesions will cause
tetraplegia (quadriplegia). Lesions at lower cervical level or below cause paraplegia or
paraparesis, with sensory loss affecting trunk and lower limbs. Cord compression also
causes neurogenic bladder involvement with bladder distension and overflow
incontinence.
Causes
l1) With cord compression
a) Spinal fractures/dislocations
b) Intervertebral disc prolapse
c) Metastatic or primary neoplasms
d) Vascular malformations
I 2) Without cord compression

a) Vascular thrombosis
b) Syringomyelia
c) Demyelinating disease
d) Nutritional deficiency (vitamin 8 , 2 )
Key Objective
• Recognise acute paraplegia as a medical emergency and identify causes
associated with cord compression.
224
• Through efficient, focused data gathering, diagnose level and cause of
paraplegia/paraparesis.
Define the upper limit of sensory loss to help determine level of injury.
Describe and explain the dissociated sensory loss and other findings in
hemi-section of the spinal cord (Brown-Sequard syndrome) and outline
other causes of paraplegia with dissociated sensory loss.
Describe the role of investigation by plain X-ray, computed tomography
(CT) scanning, magnetic resonance imaging (MRI) and isotope bone
scan in making the diagnosis of causative lesions.
225
051 Haemoptysis
Overview
Expectoration of blood can range from blood streaking of sputum to massive
haemoptysis (greater than 1,000 ml/day) that may be acutely life-threatening. Bleeding
usually starts and stops unpredictably, but under certain circumstances may require
immediate establishment of an airway and control of the bleeding.
Causes
1) Airway disease
a) Neoplasms
0 Bronchogenic carcinoma
0 Endobronchial metastatic carcinoma (melanoma, breast, renal, colon)
0 Bronchial carcinoid
0 Kaposi sarcoma (in patients with AIDS)
b) Inflammatory
0 Bronchitis (acute, chronic)
0 Bronchiectasis
c) Other (foreign body, trauma, arteriovenous fistula)
I 2) Pulmonary parenchymal disease I

a) Infectious (tuberculosis (TB), pneumonia, abscess, aspergilloma)
b) Inflammatory/Immune (Goodpasture syndrome, pulmonary
haemosiderosis, Wegener granulomatosis, lupus pneumonitis)
I 3) Vascular
a) Elevated capillary pressure (left ventricular failure, mitral stenosis)
b) Pulmonary embolus
c) Arteriovenous malformation
I4) Bleeding disorders
Is) Anticoagulant therapy
226
Tuberculosis
Key Objectives
• Determine whether the blood in sputum is true haemoptysis (originates
below the vocal cords} rather than upper respiratory tract or upper
gastrointestinal bleeding (haematemesis).
• Understand management principles for life-threatening haemoptysis.
Differentiate between the causes of haemoptysis: contrast the
disproportionate amount of blood flow in the pulmonary arteries
(virtually the entire cardiac output) to the bronchial arteries (usually two
branches off the aorta) to the origin of haemoptysis (more than 90% of
the time from the bronchial arteries).
Select investigations to determine the cause of haemoptysis (X-ray,
computed tomography (CT} scan); if arteriogram is eventually selected,
select imaging of the bronchial arteries first.
List indications for bronchoscopy.
• Conduct an effective plan of management for a patient with haemoptysis:
In the presence of massive haemoptysis (greater than 1,000 ml/day),
establish airway first and consult a specialist capable of controlling the
bleeding.
Outline the management of causes of haemoptysis which are not life-
threatening and do not require immediate referral to a specialist.
227
052 Hirsutism and Virilisation
Overview
Hirsutism is a common problem, particularly in dark-haired, darkly pigmented, white
women. However, if accompanied by virilisationJ then a full diagnostic evaluation is
essential.
Causes
1) Androgen excess (may be associated with virilisation)
a) Ovarian source
0 Polycystic ovary syndrome
0 Ovarian tumour (arrhenoblastoma)
b) Adrenal Source
0 Congenital adrenal hyperplasia
0 Cushing syndrome
0 Adrenal tumour (adenoma, carcinoma)
228
2) Drugs (usually not associated with virilisation)
a) Phenytoin
b) Antihypertensives (minoxidil)
c) Cyc losporine
3) Familial (usually not associated with virilisation)
4) Idiopathic (usually not associated with virilisation)
Key Objective
• Outline the laboratory investigation for patients with signs of androgen
excess.
Determine which patients with recent onset of hirsutism require
investigation.
Determine which patients with clinical symptoms and signs of
defeminisation (i.e. amenorrhoea) and virilisation require investigation.
Select appropriate laboratory and imaging studies.
• Conduct an effective plan of management for a patient with hirsutism and
virilisation:
Outline the medical management of patients with idiopathic hirsutism.
Outline the medical management of patients with polycystic ovary
syndrome.
Counsel and educate patients with hirsutism on conservative methods
of managing excess hair.
229
053 Hyperglycaemia I Diabetes Mellitus
Overview
Diabetes mellitus is a very common disorder. The morbidity and mortality associated
with diabetic complications may be reduced by preventive measures. Intensive
glycaemic control will reduce congenital malformations and neonatal complications in
pregnancy-associated diabetes as well as complications associated with all other forms
of diabetes.
Causes
1) Type I (beta-cell destruction insulin deficiency)
a) Immune-mediated
b) Idiopathic
12) Type II (insulin resistance)
I 3) Other specific types

a) Genetic defects (beta-cell function or insulin action)
b) Diseases of the pancreas (pancreatitis)
c) Endocrinopathies (acromegaly, Cushing syndrome)
d) Drugs (glucocorticoids, thiazides)
14) Gestational diabetes mellitus
Diabetic foot Diabetic lipoatrophy
230
Diabetic retinopathy
Key Objectives
• To diagnose diabetes mellitus and diabetic ketoacidosis.
• To provide initial management for individuals with diabetic ketoacidosis ,
and treatment-induced hypoglycaemia.
• To provide ongoing management to diabetic patients and their families.
Diagnose diabetes mellitus and associated complications.
Diagnose diabetic ketoacidosis, and hyperglycaemia-associated
hyperosmolar states and determine the precipitating causes.
processes of exclusion, differentiation, and diagnosis; and important in
formulating a differential diagnosis:
Select appropriate investigations for diagnosis of diabetes mellitus and
its complications.
hyperglycaemia I diabetes mellitus:
Outline appropriate long term management of diabetes mellitus,
including blood pressure (BP) control and primary and secondary
prevention of micro- and macro-vascular complications as well as other
complications.
Outline the management of ketoacidosis , hyperosmolar state, and
severe hypoglycaemia.
Select patients in need of specialised care and/or referral to other
Conduct education and counselling to patients with diabetes mellitus
and their families, including lifestyle modifications, and primary and
secondary prevention strategies for the complications of the disease.
231
053 Hyperglycaemia I Diabetes Mellitus
053A Hypoglycaemia
Overview
Maintenance of the blood sugar with in normal limits is essential for health. In the short
term , significant hypoglycaemia is more dangerous than hyperglycaemia.
Causes
1) Postprandial hypoglycaemia
a) Idiopathic
b) Alimentary hyperinsulinism (previous gastrectomy,
gastrojejunostomy)
I2) Fasting hypoglycaemia

a) Secondary to overutilisation of glucose
Associated with hyperinsulinism
• Exogenous insulin, sulfonylureas (including factitious
hypoglycaemia)
• lnsulinoma
• Miscellaneous drugs (pentamidine, quinine)
0 Associated with normal insulin levels
• Large extrapancreatic tumours
b) Secondary to impaired glucose production
0 Hormone deficiencies
• Adrenal insufficiency
• Hypopituitarism
0 Substrate deficiency (severe malnutrition, muscle wasting)
Drugs (alcohol, salicylate intoxication)
Enzyme defects (glucose-6-phosphatase deficiency)
0 Critical illnesses (severe hepatic failu re, cardiac disease, sepsis)
Autoimmune hypoglycaemia
232
Key Objectives
• Differentiate the causes of hypoglycaemia based on whether it occurs in
the postprandial or fasting state.
• Determine the level of awareness of hypoglycaemia in patients prone to
this condition.
Identify those patients with true hypoglycaemia.
Differentiate the cause for hypoglycaemia.
processes of exclusion, differentiation and diagnosis; and important in
Evaluate the blood sugar in patients with symptoms suggestive of
postprandial hypoglycaemia.
Outline the optimal laboratory work-up for a patient with fasting
hypoglycaemia, which will include investigation at the time of the
hypoglycaemia.
• Conduct an effective plan of management for a patient with hypoglycaemia:
Outline the management of an acute hypoglycaemic episode.
Counsel and educate patients with diabetes in relation to the symptoms
and management (as well as prevention) of hypoglycaemia.
233
054 Hypertension
Overview
Hypertension is a common condition affecting, in most countries , an increasing
proportion of the population with increasing age and is a major contributor to the global
burden of disease. A diagnosis of hypertension may require ambulatory blood pressure
(BP) monitoring or self-monitoring. Appropriate management of hypertension can
improve health outcomes. Central to an understanding of the impact of hypertension,
through its effects on the cardiovascular system, is an appreciation of the family of
cardiovascular risk factors and thei r interactions.
Causes
11) Primary (essential hypertension)
I2) Secondary
a) Renal parenchymal disease (e.g. glomerulonephritis, reflux
nephropathy, polycystic kidney disease, renal failure)
b) Syndrome X
c) Diabetes mellitus
d) Sleep-apnoea syndrome
e) Mineralocorticoid excess (e.g. adrenal adenoma or hyperplasia,
glucocorticoid-suppressible hyperaldosteronism)
f) Angiotensin II excess (e.g. unilateral renal artery stenosis)
g) Catecholamine excess (e.g. phaeochromocytoma, drugs)
h) Coarctation of the aorta
i) Endocrine disorders
(hypothyroidism, hyperthyroidism,
hyperparathyroidism (HPT),
Cushing syndrome)
j) Genetic disorders
(e.g. glucocorticoid-suppressible
hyperaldosteronism, polycystic
kidney disease, Liddle syndrome,
multiple endocrine neoplasia)
k) Drugs (sympathomimetics, cocaine,
nonsteroidal anti-inflammatory
drugs (NSAIDs), carbenoxalone,
liquorice)
Renal artery stenosis
234
Key Objective
• Avoid mislabelling patients, select patients suitable for investigation for
secondary causes, identify other cardiovascular risk factors and select the
most appropriate management for each individual with hypertension.
Diagnose hypertension and 'white coat' ('isolated clinic') hypertension.
Select patients suitable for investigation of secondary causes.
Identify end organ damage.
Characterise the patient's cardiovascular risk factor profile.
Identify hypertensive emergencies (e.g. hypertensive encephalopathy,
dissecting thoracic aortic aneurysm, malignant hypertension).
Diagnose renal parenchymal disease.
Select patients in need of specialised diagnostic care.
Discuss cost-effectiveness of investigation of hypertension.
• Conduct an effective plan of management for a patient with hypertension:
Risk stratification.
Define associated clinical conditions and comorbidities.
Set target BP levels and consider self-monitoring.
Outline non-pharmacological management strategies for patients, prior
to pharmacological ones.
Select antihypertensive medication which will not adversely affect
concomitant conditions such as diabetes mellitus, asthma, gout, and
congestive heart failure.
Select appropriate agents for hypertensive emergencies (e.g.
encephalopathy, dissection).
Communicate to patients the importance of consultation with other
healthcare professionals (e.g. dieticians).
Determine factors contributing to non-compliance and discuss possible
management strategies.
Discuss cost-effectiveness of management of hypertension.
235
054 Hypertension
054A Hypertension in Childhood
Overview
The prevalence of hypertension in children is less than one percent, but often results
from identifiable causes (usually renal or vascular). Consequently, vigorous clin ical
investigation is warranted.
Causes
1) Neonates and young infants (ischaemic or congenital renal
disease, coarctation of the aorta, hypercalcaemia, neurogenic
tumours, umbilical vessel catheterisation)
2) Children (1 to 10 years) (renal disease, both vascular and

parenchymal, coarctation, or less commonly as above)
3) Children and adolescents (11 to adolescence) (renal disease,

primary hypertension, or less commonly as above)
Key Objectives
• Perform blood pressure (BP) measurements in infants and very young
children with automated devices, and check BP tables for normal values.
• State that hypertension is a systolic or diastolic value greater than 9S'h
percentile, appropriately measured.
Diagnose hypertension and pseudohypertension; discuss 'white coat'
hypertension.
Elicit or rule out signs of secondary hypertension.
236
Outline value and use of ambulatory BP monitoring.
Select patients in need of diagnostic imaging and other laboratory
investigation.
• Conduct an effective plan of management for a paediatric age group patient
with hypertension:
Outline for patients dietary treatment only if obese.
Select antihypertensive medication and dose.
encephalopathy, cardiac failure) .
237
054 Hypertension
0548 Pregnancy-Associated Hypertension
Overview
Preeclampsia is generally a self-limited disease with rapid resolution of hypertension
and a low recurrence rate in future pregnancies (less than 7%). However, when severe,
and especially when it occurs in the second trimester, preeclampsia is not so benign.
Such patients are at high risk for recurrence in subsequent pregnancies (as high as
65% when the preeclampsia is in the second trimester) and also at high risk for
hypertension later in life. The incidence of fetal growth retardation is about 10%.
Causes
1) Pregnancy-induced hypertension
a) Preeclampsia
b) Eclampsia
2) Chronic (pre-existing) hypertension I Chronic renal disease

a) Preeclampsia superimposed on chronic hypertension
Key Objectives
• Describe the normal changes of blood pressure (BP) in pregnancy and
define hypertension in pregnancy with these changes in mind.
• Outline the treatment of preeclampsia including consideration for early
diagnosis, medical supervision, and timely delivery. This should include:
Control BP.
Assess maternal condition - urine, blood tests required .
Look tor underlying medical condition.
Assess fetal condition.
Prevent eclampsia.
Delivery - timing and mode.
238
Differentiate preeclampsia from chronic hypertension and transient
hypertension.
Elicit symptoms and signs indicative of risk for eclampsia (e.g.
headache, epigastric pain, visual abnormalities, proteinuria).
Select and interpret laboratory investigation useful to the diagnosis of
preeclampsia and 'HELLP' syndrome (l::faemolysis, &levated Liver
enzymes, .Low Platelets).
• Conduct an effective plan of management for a patient with hypertension in
pregnancy:
Discuss the goals of management of hypertension in pregnancy (first,
with respect to the safety of the mother, and second, the delivery of a
live infant not requiring intensive, prolonged neonatal care) as listed in
Key Objectives above.
Discuss strategies for the prevention of pregnancy-induced
hypertension.
List drugs indicated and contraindicated in the management of
hypertension in pregnancy.
Hypertensive retinopathy
239
054 Hypertension
054C Hypertension in the Elderly
Overview
Elderly patients (older than 60-65 years) have hypertension much more commonly
than younger patients do, especially systolic hypertension. T he prevalence of
hypertension among the elderly may reach 60%-80%.
Causes
Causes are the same as for hypertension in younger patients, but if age more than
50 years, secondary hypertension becomes more likely.
1) Primary hypertension
(see #054 Hypertension)
I 2) . Secondary hypertension
(see #054 Hypertension)
Key Objectives
• Define hypertension in the elderly in a manner similar to younger patients;
define pseudohypertension.
• Conduct antihypertensive pharmacologic treatment for systolic
hypertension in elderly patients when systolic blood pressure (BP) is
consistently greater than 160 mm Hg (use standing BPs as a guide to
therapy) , since evidence of benefit exists.
• State that the benefit of treating hypertension in the elderly is two to four
times greater than that achieved in the treatment of younger patients with
primary hypertension.
Diagnose hypertension and pseudohypertension.
Select patients suitable for investigation of secondary causes.
Identify end organ damage.
Identify hypertensive emergencies (e.g. hypertensive encephalopathy,
dissecting aortic aneurysm, malignant hypertension, transient ischaemic
attacks).
Select patients in need of specialised diagnostic care.
240
• Conduct an effective plan of management for an elderly patient with
hypertension:
Outline for patients non-pharmacological management strategies prior
to pharmacological ones.
Select antihypertensive medication which will not adversely affect
concomitant conditions such as diabetes mellitus, asthma, and
congestive heart failure .
encephalopathy, dissection).
Communicate to patients the importance of consultation with other
healthcare professionals (e.g. dieticians).
Determine factors contributing to non-compliance and discuss possible
management strategies.
Discuss cost-effectiveness of management of hypertension in the
elderly.
Define the goals of treatment in elderly hypertensive patients and
contrast these with the goals for younger patients.
241
054 Hypertension
054D Malignant Hypertension
Overview
Malignant hypertension and hypertensive encephalopathy are two life-threatening
syndromes caused by marked elevation in blood pressure (BP).
Causes
1) Primary hypertension (longstanding, uncontrolled, drug
withdrawal)
I2) Sec!lndary hypertension

a) Increased cardiac output (secondary increase in vascular resistance)
0 Chronic renal failure, uraemia with volume overload
0 Acute renal disease (glomerulonephritis, scleroderma crisis)
0 Primary hyperaldosteronism (Conn syndrome)
b) Increased vascular resistance
0 Renovascular hypertension (renal artery stenosis)
0 Phaeochromocytoma
0 Drugs (cocaine, food or drug interactions with monoamineoxidase
inhibitors, nonsteroidal anti-inflammatory drugs (NSAIDs))
Key Objectives
• Differentiate primary malignant hypertension (marked hypertension with
diastolic BP usually greater than 140 mm Hg, associated with grade three
to four retinopathy, proteinuria and renal impairment) from secondary
conditions such as uraemia with flu id overload, subarachnoid or cerebral
haemorrhages, brain tumours, head injury, seizure, etc.
• Conduct initial hypertension lowering treatment in a manner which lowers
the BP gradually over hours, not precipitously.
Determine quickly whether other hypertensive emergencies are present
(e.g. aortic dissection, acute pulmonary oedema, acute or impending
myocardial infarction (MI), cerebrovascu lar events) and make BP
lowering the first concern.
Once BP control is in place, diagnose the cause of the BP elevation.
242
Have an appropriate investigation strategy, since certain medications
can interfere with some biochemical tests.
• Conduct an effective plan of management for a patient with malignant
hypertension:
Recognise that the control of BP in a patient with malignant
hypertension usually requires admission to an intensive care unit (ICU).
Outline the immediate management of malignant hypertension with
parenteral drugs with intra-arterial BP monitoring in an ICU setting and
with other medications if an ICU is not available.
Discuss advantages and disadvantages of various BP-Iowering drugs
used in malignant hypertension and other hypertensive emergencies.
Describe and explain the potential hazards of too rapidly lowering BP
levels below 100- 105 mm Hg diastolic or greater than 25% of baseline.
Outline a long term management strategy.
Malignant hypertension retinopathy
243
055 Infertility I Impotence I Sexual Dysfunction
Overview
Infertility affects about 10-15% of couples. Both partners should be investigated
simultaneously since male-associated factors account for at least one-third of infertility
problems, and problems are often identified in both male and female partners.
Causes
1) Infertility
a) Female
(see #063 Menstrual Cycle Abnormal)
0 Disorders of ovulation - causes at level of hypothalamus, pituitary, or
ovary
Disorders of tubal function
0 Other causes - fibroids , endometriosis
b) Male - disordered semen specimen
0 Endocrine causes - hypothalamic/pituitary causes
(panhypopituitarism, haemochromatosis) - may have associated
decreased androgenisation.
Testicular (viral orchitis, radiation, drugs, liver disease, renal failure)
0 Varicocele
u Abnormal sperm transport (obstruction of vas deferens)
I 2) Impotence
a) Endocrine causes (testicular failure, hyperprolactinaemia)
b) Drugs (spironolactone, thiazides, beta-blockers, tricyclics, alcohol)
c) Neurologic diseases
0 Diseases of spinal cord
Polyneuropathy I Autonomic neuropathy (diabetes)
d) Vascular disease
Atherosclerotic occlusion of cavernous or pudenda arteries
Venous leak
e) Psychogenic
244
Key Objectives
• Outline the investigation for couples with infertility.
• Outline the therapeutic options for couples with infertility.
Diagnose the most likely cause of infertility.
Determine which patients are likely to have an organic cause for their
impotence.
Order and interpret a semen analysis.
Outline the laboratory investigation of a female with infertility.
• Conduct an effective plan of management for a patient with infertility or
impotence:
Outline the medical and surgical management of a female/couple with
infertility, considering the various causes of infertility and the treatment
modalities for each (including the use of modern reproductive
techniques of invitro-fertilisation (IVF) I intra-cytoplasmic sperm injection
(ICSI) and gamete donor use).
Determine the therapy for impotence based on the underlying cause.
Describe the role of specific injectable and oral medications and the
potential for surgical correction in patients with erectile dysfunction.
Counsel and educate couples with infertility including the option of
adoption.
245
056 Insomnia I Sleep and Circadian Rhythm Disorders I
Sleep-Apnoea Syndrome
Overview
Insomnia is a symptom that affects one-third of the population at some time, and is a
persistent problem in 10% of the population. Affected patients complain of difficulty in
initiating and maintaining sleep, and this inability to obtain adequate quantity and quality
of sleep results in impaired daytime functioning .
Causes
j 1) Transient and short term insomnia
a) Change in sleeping environment I Excessive noise I High or low
ambient temperature
b) Jet-lag
c) Change in work shift
d) Stressful life events I Acute illness
e) Stimulant medication (theophylline, steroids, beta-agonists,
thyroxine)
I 2) Chronic insomnia
a) Psychiatric disorders (depression, anxiety disorders, schizophrenia)
b) General medical disorders
Cardiac (heart failure , coronary artery disease (CAD))
0 Respiratory (chronic obstructive pulmonary disease (COPD), asthma)
0 Gastro-intestinal (reflux, peptic ulcer disease)
0 Arthropathies I 'Fibromyalgia' I Lyme disease
0 AIDS
0 Chronic fatigue syndrome
c) Neurologic
Strokes (central hemispheric and brain stem)
Neuro-degenerative (Alzheimer disease, Parkinson disease)
0 Brain tumours
0 Neuromuscular (painful neuropathies)
Headaches (see #046 Headache)
Fatal familial insomnia
d) Drug/Alcohol insomnia
246
e) Primary sleep disorders
0 Primary or idiopathic
tJ Psycho-physiologic
U Sleep state misperception
0 Circadian rhythm disorders
• Delayed sleep phase syndrome
• Advanced sleep phase syndrome
• Hypernychthemeral syndrome
U Restless legs syndrome I Periodic limb movement disorder
u Altitude insomnia
0 Insufficient sleep syndrome
0 Central sleep-apnoea syndrome
Key Objective
• Elicit a history of sleep habits involving the entire 24-hour cycle , including
history from bed partner or caregiver (sleep habits, drug/alcohol
consumption , medical or psycho-neurologic disease, psycho-social
stressors, etc.).
• Throug h efficient, focused data gathering:
Conduct an examination of the patient to detect concomitant medical
conditions which can adversely affect sleep.
Describe to the patient a 'sleep log' and request one.
State that laboratory investigation is not required in the routine
evaluation of insomnia.
List situations for which polysomnography may be indicated.
• Conduct an effective plan of management for a patient with insomnia:
State that management depends on the underlying cause.
Outline some non-pharmacologic strategies for management of
idiopathic chronic insomnia.
State that pharmacologic therapy is generally not the treatment of first
choice and should always be combi ned with non-pharmacologic
therapies (e.g. sleep hygiene).
247
057 Involuntary Movement Disorders I Tic Disorders
Overview
Motor function may be impaired in a number of different ways, involving either a paucity
or an excess of movements. Abnormal movements may be spontaneous (at rest),
postural, or only with intention. They may involve dyskinesias, choreoathetosis, tremors,
tics, myoclonic jerks or fascicu lations.
Causes
1) Akinesia (Parkinson disease: idiopathic or drug-induced)
2) Rigidity (Parkinson disease: idiopathic or drug-induced)
3) Akathisia (drug-induced, Parkinson disease, delirium)
4) Chorea (hereditary, basal ganglia disease, Huntington disease,

rheumatic chorea, thyrotoxicosis, systemic lupus
erythematosus (SLE), neuroleptics, pregnancy, polycythaemia)
5) Athetosis (cerebral palsy, Wilson disease, cerebral anoxia)
6) Hemiballismus (contralateral subthalamic pathology,

hypertension, diabetes mellitus)
I 7) Dystonia
a) Primary (idiopathic, inherited)
b) Secondary (kernicterus, Wilson disease, heavy metals, cerebral
anoxia, drug-induced)
c) Focal (spasmodic torticollis, cranial, occupational, drug-induced)
I 8) Myoclonus
a) Physiological (sleep, anxiety, exercise, hiccough)
b) Essential (familial, sporadic)
c) Epileptic (benign, infantile, progressive, petit mal)
d) Symptomatic (encephalopathy, basal ganglia disease, dementias,
metabolic, toxic, physical, focal central nervous system (CNS)
damage).
19) Tremor
a) Familial/Essential
b) Physiological (anxiety, fatigue, alcohol, caffeine)
c) Orthostatic
d) Symptomatic (Parkinson disease, cerebellar disease)
248
10) Restless legs syndrome
11) Asterixis (metabolic/hepatic)
12) Habit spasms and tics (Tourette syndrome)
Key Objectives
• Describe the abnormal movement accurately after careful observation both
at rest and in action.
• Conduct appropriate testing to exclude treatable conditions:
Wilson disease, thyrotoxicosis, SLE, heavy metal poisoning, carbon
monoxide poisoning and syphilis, etc.
• Be aware of common drug-induced causes of involuntary movements:
Neuroleptics, anticholinergics, antidepressants, antipsychotics, lithium,
1-dopa, haloperidol, thyroxine , caffeine, alcohol, bromocriptine.
• Through efficient, focused data gathering and neurological examination:
Differentiate between the various causes of movement disorders.
• Interpret critical clinical and laboratory findings which were crucial in the
Select patients in need of referral for investigation or specialised care.
Conduct testing for Wilson disease.
• Develop an effective management plan for a patient with an involuntary
movement disorder I tic disorder.
• Contact family members and consider screening if either Wilson disease,
Huntington disease or Tourette syndrome is diagnosed.
2 49
058 Jaundice
Overview
Jaundice is not usually detectable clinically until the serum bilirubin is greater than
30 mmoi/L. Excess haemolysis causes mild acholuric jaundice (bilirubin attached to
albumin does not appear in the urine) whereas cholestatic jaundice is associated with
dark urine (conjugated bilirubin passes through the kidneys into the urine). Dark urine
is usually the first symptom in cholestatic jaundice. Jaundice resulting from hepatobiliary
disease may represent a benign heritable condition or severe life-threatening disease.
Causes
1) Unconjugated hyperbilirubinaemia
a) Overproduction
0 Haemolysis
0 Ineffective erythropoiesis
b) Decreased hepatic uptake (sepsis)
c) Decreased bilirubin conjugation
0 Hereditary transferase deficiency (Gilbert syndrome, Crigler-Najjar
syndrome)
0 Neonatal jaundice
0 Acquired transferase deficiency (breast milk, hepatocellular disease)
I2) Conjugated hyperbilirubinaemia

a) Intrahepatic cholestasis
0 Drugs (erythromycin, oral contraceptive pill (OCP))
0 Hepatocellular disease (hepatitis)
0 Cirrhosis
• Infectious diseases including postviral
• Hereditary diseases (alpha-1-antitrypsin deficiency,
haemochromatosis, Wilson disease)
• Primary biliary cirrhosis
• Alcohol
0 Miscellaneous (fatty liver, sepsis)
b) Extrahepatic cholestasis
0 Intraductal obstruction
• Gallstones
• Sclerosing cholangitis
• Biliary malformation (stricture)
• Malignancy (cholangiocarcinoma)
0 Compression of biliary ducts (malignancy)
250
Key Objectives
• Determine which patients have significant liver dysfunction and evaluate
the progression of the jaundice.
• Appreciate that alcohol is the commonest cause of cirrhosis.
• Through efficient. focused data gathering:
Differentiate between the various causes for jaundice and determine
which are treatable.
Describe and demonstrate complications related to the presence of liver
disease.
Indicate changes in the sclera, skin, urine and faeces with the various
causes.
Select and interpret appropriate investigations for patients with
jaundice.
Order and interpret a blood smear in patients with unconjugated
hyperbilirubinaemia.
List the indications for and interpret an abdominal ultrasound including
the significance of dilated bile ducts.
• Conduct an effective plan of management for a patient with jaundice:
Outline a management plan for common causes of jaundice.
Outline a management plan for patients with acute hepatic failure.
Select patients in need of specialised care and/or in need of urgent
hospitalisation.
251
058 Jaundice
OSSA Neonatal Jaundice
Overview
Jaundice is the most prevalent problem in the newborn period; up to 65% of full-term
neonates develop transient jaundice. Although some causes are ominous, the majority
are transient and without consequences. Physiologic jaundice comprises a transient
decrease in the conjugation of bilirubin, appears on the second or third day of life and
disappears within two weeks.
Causes
1) Unconjugated hyperbilirubinaemia
a) Increased bilirubin production
0 Haemolytic causes - Coombs positive
• lsoimmune (Ah and ABO blood types , other blood antigens),
autoimmune (systemic lupus erythematosus (SLE))
• Acquired red cells defects (e.g. drugs)
0 Haemolytic causes - Coombs negative
• Red cell membrane defects (elliptocytosis, pyknocytosis, etc.)
• Red blood cell (ABC) enzyme deficiencies (pyruvate kinase,
glucose-6-phosphate dehydrogenase)
• Haemoglobinopathy (with or without thalassaemia)
• Microangiopathy (haemolytic-uraemic syndrome)
b) Decreased bilirubin conjugation
0 Metabolic/Genetic (Gilbert syndrome, Crigler-Najjar syndrome,
hypothyroidism)
0 Physiologic jaundice I Breast milk jaundice
c) Gastrointestinal absorption (pyloric stenosis, meconium ileus,
sequestered blood)
j 2) Conjugated hyperbilirubinaemia
a) Decreased bilirubin uptake
0 Infections (sepsis, neonatal hepatitis) I Toxic (parenteral nutrition)
0 Metabolic/Genetic (galactosaemia, Gaucher disease, Niemann-Pick
disease, decreased Y protein)
b) Decreased bilirubin excretion I Obstructive (biliary atresia,
obstruction, choledochal cyst)
252
Key Objectives
• Determine whether jaundice presented at birth or within 24 hours, as in
general such presentation is pathologic.
• State that hyperbilirubinaemia is most threatening when the onset is rapid ,
and the bilirubin is unconjugated. In the relatively immature central
nervous system (CNS) of the neonate, especially in the premature,
unconjugated bilirubin may be deposited and can result in severe brain
damage.
Elicit a history regarding family history of haematological disorders,
previously affected children , maternal blood type, and antibody status,
delivery history, how colouration was noticed, vital signs, and any
medications.
Perform examination of scleral and mucous membranes, skin, liver and
spleen, ascites, circulatory status, urine and stool.
Differentiate physiologic from organic causes of neonatal jaundice.
Select investigations that will differentiate conjugated from
unconjugated hyperbilirubinaemia.
Select investigations that will differentiate pathologic
hyperbilirubinaemia from exaggerated physiologic jaundice.
State that conjugated hyperbilirubinaemia is never physiologic and
select tests for immediate investigations.
• Conduct an effective plan of management for a neonatal patient with
jaundice:
Outline initial monitoring and management in neonatal jaundice.
Explain advantages and disadvantages of phototherapy, exchange
blood transfusions , and pharmacologic therapy.
Select appropriate consultants in the management of neonatal jaundice.
253
059 Joint Pain, Mono-Articular (Acute, Chronic)
Overview
Pain involving a single joint, with painful limitation of movement, is a common presenting
symptom. Conditions such as an infective arthritis are important to identify since failure
to make the correct diagnosis could lead to permanent harm to the patient.
Causes
1) Infection (bacterial, mycobacterial, fungal, viral, spirochaetes)
I 2) Crystal (gout, pseudogout)
3) Haemarthrosis (trauma/fracture, anticoagulants 1 bleeding

disorders)
I 4) Tumour (osteoma, sarcoma)
5) Systemic rheumatic disease (rheumatoid arthritis (RA),

systemic lupus erythematosus (SLE), sarcoid)
16) Osteoarthritis (erosive variant)
Key Objectives
• Evaluate a patient with mono-articular arthritis first for the possibility of
infection, since this relatively common cause of acute pain and swelling in a
single joint can result in cartilage destruction within a few days if
unrecognised.
• Recognise that the differential diagnosis of mono-articular arthritis overlaps
with that of poly-articular arthritis, initially presenting as a single swollen
joint.
254
Differentiate articular from non-articular disorders.
After considering infection, diagnose other causes of mono-arthritis.
Select appropriate investigations including diagnostic joint aspiration
and synovial flu id analysis.
• Conduct an effective plan of management for a patient with mono-articular
joint pain:
Outline appropriate treatment of septic arthritis.
Select appropriate treatment for other causes of arthritis.
List the indications, contraindications, and adverse effects of drugs
commonly used in the treatment of arthritis (e.g. nonsteroidal anti-
inflammatory agents).
255
060 Joint Pain, Poly-Articular (Acute, Chronic)
Overview
Poly-articular joint pain ('polyarthralgia') is common in medical practice, and causes
vary from some that are self-limiting to others which are potentially disabling and life-
threatening. The term 'arthritis' includes inflammatory, infective, and degenerative joint
disease. Arthritis is usually characterised by the spontaneous development of pain
exacerbated by joint movement; and in superficial joints is often associated with swelling
of the joints.
The most common types of arthritis seen in Australia are degenerative osteoarthritis
and rheumatoid arthritis.
Causes
11) Degenerative osteoarthritis
2) Infectious (Lyme disease, bacterial endocarditis,

gonococcus, viral)
13) Post-infectious (reactive)

a) Rheumatic fever
b) Reiter syndrome
c) Enteric infections
4) Seronegative spondyloarthritides
I 5) Systemic rheumatic diseases

a) Rheumatoid arthritis (RA)
b) Systemic lupus erythematosus (SLE)
c) Systemic vasculitis
d) Systemic sclerosis
e) Polymyositis I
Dermatomyositis
Juvenile rheumatoid arthritis Rheumatoid arthritis - swan neck deformities
256
Rheumatoid nodules
6) Other (sarcoidosis, inflammatory osteoarthritis)
Key Objectives
• Differentiate articular from non-articular pain by clinical criteria; and
between inflammatory and noninflammatory arthritis.
• Determine whether the patient has a musculoskeletal or neurologic
emergency, compartment syndrome or acute myelopathy, versus
radiculopathy or neuropathy.
• Differentiate neurologic causes by the burning quality associated with
numbness, paraesthesia, constancy, worse at night, and unrelated to
motion.
Differentiate between inflammatory and non-inflammatory arthritis.
Describe articular and extra-articular manifestations and complications.
process of exclusion, differentiation, and diagnosis:
Select and interpret investigations including synovial fluid analysis.
• Conduct an effective plan of management for a patient with poly-articular
joint pain:
Outline the principles of multidisciplinary management of RA and other
inflammatory and non-inflammatory arthritides.
Outline a management plan for patients with inflammatory and non-
inflammatory arthritis including drug therapy, physiotherapy,
occupational therapy, and treatment of joint deformities.
Conduct counselling and education of patients.
257
061 Limp 1 Pain in Lower Extremity in Children
(See also N089G Hip Pain, N089H Knee Pain}
Overview
Growing pains is a general diagnosis that is being made less frequently as clinicians
become more expert in making specific diagnoses. Although growing pains do exist as
a form of myalgia, the clinician's aim should be to make as specific a diagnosis as
possible.
Causes
1) Trauma (stress fracture, traumatic epiphyseal injury)
(see #041 Fractures I Dislocations)
2) Infections (septic arthritis, osteomyelitis)

(see #071 Painful Limb)
3) Inflammatory Uuvenile rheumatoid arthritis (RA), reactive

arthritis, toxic synovitis of hip)
14) Other
a) Hip
0 Legg-Calve-Perthes disease
0 Slipped capital femoral epiphysis
b) Knee
Osgood-Schlatter disease or epiphysitis
0 Chondromalacia patellae
0 Patella (tendon partial rupture, osteochondritis, subluxation,
dislocation)
Meniscal injuries
Popliteal cyst
Is) Growing pains
258
Perthes disease
-
Key Objectives
• Determine whether the pain originates in joints or soft tissue.
• Recognise that the most serious diseases causing leg pain in children are
usually unilateral.
• Through efficient, focused , data gathering:
Communicate to child and parents that pain or limp lasting for longer
than two to three weeks is unlikely to be the result of trauma even in the
presence of trauma history.
Determine if the limp or pain are caused by serious entities.
Calculate leg length discrepancies (greater than 1 em may cause pelvic
tilt and limp), describe gait.
Select patients in need of diagnostic imaging or specialised care for
further investigation.
• Conduct an effective plan of management for a child with pain in the lower
extremity and/or limp:
259
062 Lymphadenopathy
Overview
Patients with focal lymphadenopathy at one site (groin, axilla, neck, abdomen) require
careful assessment initially to identify neoplastic or inflammatory causes within regional
fields. Generalised lymphadenopathy requires search for malignant or inflammatory
disease. Finally, aspiration cytology is often diagnostic in the assessment of the lymph
node swellings. Lymph nodes may be normally palpable in the groin, axilla or neck,
but a lymph node swelling of 2 em or greater which is persistent and firm , demands
investigation.
Causes
1) Localised
a) Infectious causes
Bacterial (streptococci, staphylococci, cat scratch, tuberculous)
0 Viral (herpes simplex)
b) Reactive (usually secondary to undiagnosed infection)
c) Malignant diseases
0 Metastatic disease
0 Localised lymphoma
Cervical abscess following tonsillitis
Trolsier sign - CIJICinoma

stomach
Metastasis from pharyngeal cancsr
260
I 2) Generalised
a) Infectious causes
0 Viral (Epstein-Barr virus (EBV}, cytomegalovirus (CMV), infectious
hepatitis, rubella, HIV)
0 Bacterial (brucellosis)
0 Fungal (histoplasmosis, coccidioidomycosis)
b) Inflammatory diseases
0 Collagen diseases (rheumatoid arthritis (RA), systemic lupus
erythematosus (SLE}, dermatomyositis, Sjogren syndrome)
0 Serum sickness
0 Drug hypersensitivity (allopurinol, phenytoin)
0 Sarcoidosis
0 Amyloidosis
c) Malignant diseases
0 Lymphoma
0 Acute or chronic lymphocytic leukaemia
Key Objective
• Differentiate the cause of lymphadenopathy based on its location and
distribution.
Differentiate benign from malignant causes for lymphadenopathy.
• Interpret critical cl inical and laboratory findings which were key in the
Outline the laboratory investigation for a patient with generalised
lymphadenopathy.
List the indications for a lymph node biopsy.
lymphadenopathy:
Determine which patients require further investigation for their
lymphadenopathy.
261
063 Menstrual Cycle Abnormal
063A Amenorrhoea (also Oligomenorrhoea}
Overview
The average age of menarche is less than 13 years (1 1- 15 years). Most young women
(phenotypic) failing to develop menses simply have delayed menarche, but rarely some
(older than 16-17 years) fail to menstruate at all (primary amenorrhoea). Patients who
have menstruated but have stopped (more than four to six months), have secondary
amenorrhoea (commonest cause during reproductive years is pregnancy).
Oligomenorrhoea investigation should include important issues such as nutrition and
medications.
Causes
Primary amenorrhoea, secondary amenorrhoea and oligomenorrhoea. The causes
which only apply to primary amenorrhoea are marked with an asterisk(*). The others
can apply to all of these causes.
1) Pregnancy (also gestational trophoblastic tumours)
I 2) Endocrine causes:
a) Hypothalamic - physiologic (exercise, stress, weight loss or gain,
drugs) - pathologic - tumour
b) Pituitary -tumour or hypopituitarism (including Sheehan syndrome)
c) Thyroid - underactivity, overactivity
d) Adrenal - congen ital adrenal hyperplasia, tumour
e) Ovarian- polycystic ovary syndrome, ovarian failure, ovarian
agenesis*, streak gonads (45X)*, hormone-producing ovarian tumour
3) Uterine/Outflow tract anatomic defects

a) Congenital absence of vagina* / Imperforate hymen*, transverse
vaginal septum*
b) Cervical stenosis
c) Intra-uterine adhesions I Uterine absence* I Mal-development I
Asherman syndrome
262
Key Objective
• First determine whether the woman is pregnant if aged 10-50 years; order
a pregnancy test. If not pregnant, consider other diagnoses. Be aware of
special causes of primary amenorrhoea.
Determine degree of maturation of breasts, pubic and axillary hair, and
external genitalia.
Determine current oestrogen status and presence or absence of outflow
tract anatomic defect.
Determine patient's diet, drugs, and stress level; presence of
galactorrhoea, hirsutism, acne.
List indications for serum prolactin, gonadotropins, oestrogen and
progesterone investigations.
List indications for obtaining a chromosomal karyotype.
List indications for assessing androgen status and what tests should be
done.
List indications for a pelvic ultrasound examination.
• Conduct an effective plan of management for a patient with amenorrhoea:
Outline a management plan in a patient with functional hypothalamic
amenorrhoea, including a rational basis for the agents used to induce
ovulation if pregnancy is desired, and the place for hormone
replacement therapy (HAT) if pregnancy is not desired.
Outline a management plan for a patient with ovarian failure , consider
'pros' and 'cons' of HAT.
263
063 Menstrual Cycle Abnormal
0638 Pre-Menstrual Syndrome I Dysmenorrhoea
Overview
Approximately 30- 50% of post-pubescent women experience painful menstruation and
10% of women are incapacitated by pain one to three days per month. Dysmenorrhoea
is the single greatest cause of lost working hours and school days among young women.
Causes
11) Pre-menstrual syndrome
I 2) Dysmenorrhoea
a) Primary (no pelvic abnormality)
b) Secondary (acquired)
0 Fibroids
0 Endometriosis
0 Infections I Foreign body
0 Cervical occlusion
0 Congenital abnormalities
Key Objective
• Differentiate primary (within the first two to three years of menarche, with
regular ovulatory menstruation) from secondary dysmenorrhoea (usually
many years after menarche).
264
Differentiate between pre-menstrual syndrome (pain and other
symptoms 2-12 days before, and improve with menses), and
dysmenorrhoea.
Differentiate between primary and secondary dysmenorrhoea.
Perform pelvic examination to diagnose possible causes of secondary
dysmenorrhoea.
Order Papanicolaou (Pap) smear, wet smear, cultures.
Select patients in need of referral for additional investigation.
• Conduct an effective plan of management for a patient with pre-menstrual
syndrome or dysmenorrhoea:
Outline initial management of pre-menstrual syndrome or
dysmenorrhoea.
265
064 Menopause
Overview
Women live about one-third of thei r lives after ovarian function ceases. As the population
ages, quality of life and d isea~e _pr~v~ntion strategies are inherent in managing the
post-menopausal symptoms in women.
Causes
1) Physiologic
a) Oocytes responsive to gonadotropins progressively disappear from
the ovaries
b) Oocytes do not respond to gonadotropins- ovarian resistance
I 2) Pathologic or induced
a) Infections or tumours of reproductive tract resulting in destruction or
removal of a significant amount of ovarian tissue
b) Ionising radiation
c) Chemotherapy (cytotoxic agents)
d) Surgery impairing ovarian blood supply
e) Autoimmune or other processes disturbing ovarian function
Key Objectives
• Counsel women with menopause that nothing can prevent physiologic
menopause (ovarian function cannot be prolonged indefinitely) and nothing
can be done to postpone its onset or slow its progress. However, reassure
patient that sudden ageing will not occur, sexual activity can continue , and
hormone replacement therapy (HAT) can prevent many of the adverse
effects seen.
• Explain the physiologic events being experienced by a woman in
menopause in order to dispel fears and assess symptoms such as anxiety,
depression, or sleep disturbance.
• State that osteoporosis is one of the most important health hazards
associated with the menopause, along with an increase in coronary artery
disease (CAD), Alzheimer disease, macular degeneration of the retina ,
urinary continence problems and bowel malignancy (all have a lesser
incidence in women taking HAT).
266
Differentiate from other causes of amenorrhoea (see #063 Menstrual
Cycle Abnormal, #117 Vaginal Bleeding, Excessive in Amount or
Irregular in liming and #118 Vaginal Discharge I Urinary Symptoms,
Vulvar Lesions, Sexually Transmitted Diseases (STDs)).
Determine whether there has been a decrease in amount and duration
of menstrual flow, tapering to spotting, or cessation ; determine length of
time since onset of amenorrhoea.
Determine whether there are symptoms associated with vaginal
changes to exclude other pathology (brownish discharge, bleeding with
coitus, vaginal pruritus or leucorrhoea, excessive vaginal dryness,
dyspareunia).
Elicit history of urinary tract symptoms, change in breasts, hot flush ,
cardiovascular symptoms, skin and hair changes, or any psychological
complaints.
Perform a diagnostic pelvic examination.
Obtain a relevant family history regarding risks of cancer, osteoporosis
and cardiovascular disease.
Select patients requiring cytologic smears, hormone measurements, or
bone density studies.
• Conduct an effective initial plan of management for a patient with
menopause:
Counsel patients regarding prevention of osteoporosis, advantages and
disadvantages of oestrogen replacement (e.g. endometrial cancer,
breast cancer, hepatic function, hypertension, thromboembolic disease,
lipid metabolism).
List contraindications to HAT.
Outline guidelines for hormonal (or oestrogen and progestin)
replacement therapy.
List alternatives to oestrogen therapy for some of the symptoms of
menopause.
287
065 Mood Disorders
Overview
Depressive illness is one of the commonest illnesses in medicine and is often confused
with other illnesses. Depressed and anxious patients often present to doctors with
somatic symptoms used as 'tickets-of-entry' , when their primary disorders are
psychological.
Although the return to the pre-depressive state, either spontaneously or with treatment,
is the rule , untreated depressive episodes may last six months, they are usually
recurrent, and chronic outcomes are not rare.
Bipolar disorders are episodic recurrent illnesses which have an onset at an early age
and with a great deal of variation in cycling patterns.
Causes
1) Major depression
a) With melancholic features
b) With psychotic features
c) Postpartum
d) Seasonal
e) Atypical
f) Recurrent
12) Dysthymia
13) Cyclothymic disorder
14) Bipolar I disorder

a) Hypomanic
b) Manic
c) With psychotic features
d) Postpartum
e) Seasonal
f) Rapid cycling
g) Mixed
Is) Bipolar II disorder

a) Hypomanic
b) Depressed
c) Melancholic
d) Atypical
e) Postpartum
268
6) Adjustment disorder with depressed mood
7) Mood disorder due to ·a medical condition

a) Depressed (drugs, neoplasms, endocrine, cerebrovascular disorder)
b) Manic/Hypomanic (drugs, infections, neoplasms, metabolic
disorders, epilepsy)
c) Mixed
8) Substance-induced mood disorder (amphetamines, cocaine,

cannabis, hallucinogens)
a) Depressed
b) Manic/Hypomanic
c) Mixed
d) When intoxicated
e) During withdrawal
19) Schizoaffective disorders -}

a) Bipolar
b) Depressed
Key Objectives
• Differentiate between the presence of one of the mood disorders (illness)
and normal (non-illness) conditions such as bereavement and periods of
sadness.
• Recogn ise the depressed patient at risk of suicide.
Ge neral/Specific Objectives
Determine the intensity, duration (weeks, years) of depression and its
effect on function (loss of interest in all activities, change in sleep,
appetite, libido, energy).
Determine whether a general medical condition is present, use or abuse
of drugs (or withdrawal).
Elicit history of sense of worthlessness, excessive guilt, inability to
concentrate, suicidal thoughts.
Exami ne for slowness of thought, speech, motor activity or signs of
agitation such as fidgeting, moving about, hand-wringing, nail-biting,
hair-pu lling, lip-biting; examine vital signs, pupils, and skin for previous
suicide attempts, stigmata of drug and/or alcohol use, thyroid gland.
Elicit history of elevated mood, expansive or irritable mood (for at least
one week) with impairment in function or without impairment and lasting
only four days.
2 69
Select patients only when high index of suspicion requires further
investigation for medical condition or drugs that affect mood (e.g.
thyroid function , toxicology screen, serum electrolytes, liver function
tests).
• Conduct an effective plan of management for a patient with mood
disorders:
Outline and describe treatments available for mood disorders under
categories of medications, physical treatment, and psychologic
treatment.
270
066 Mouth Problems
Overview
Although many disease states can affect the mouth, the three most common and most
important ones are: dental caries, gingivitis, and oral carcinoma.
Causes
1) Sore mouth problems in children I
a) Abnormalities in teeth (caries from pacifiers, eruptions, number, form,
size)
b) Trauma (accidents, child abuse)
c) Gingival overgrowth (idiopathic, genetic, drugs)
I 2) Mouth problems in adults

a) Dental caries I Periapical dental abscess I Cellulitis (emergency)
b) Gingivitis I Periodontal I General mouth diseases
0 Oral hygiene
0 Systemic factors (haematological disorders, HIV)
0 Sexually transmitted I blood-borne infections
c) Mouth ulcers / Lip lesions
0 Acute, painful (aphthous), herpetic
0 Chronic persisting
• Malignant (squamous cell, muco-epidermoid, basal cell)
• Pre-malignant (leukoplakia, erythroplakia)
271
d) Pigmented lesions in the mouth
0 Tobacco, Betel nut
0 Lead, bismuth, iron
0 Drugs (antimalarials, oral contraceptive pill (OCP))
0 Addison disease
0 Peutz-Jeghers syndrome
0 Melanoma
e) Other (cellulitis, trauma, Candida)
f) Salivary glands (mumps, bacterial infections, sialolithiasis, tumour,
mucuos cyst)
13) Mouth problems in the elderly

a) Receding gingivae/gums
b) Edentulism
Malignant ulcer tongue
Leukoplakia tongue
Peutz-Jeghers syndrome Mucous cyst
272
Key Objectives
• Select patients for referral to dentist for caries/abscess/cellulitis as well as
regular prophylactic care.
• Select patients for referral to ear, nose and throat (ENT) specialist for any
indurated lesions.
Elicit history of tobacco (smoking or chewing) or large quantities of
alcohol or spices and perform examination of the mouth including
direct visualisation and palpation of the teeth and the entire surface
searching for painless plaque, ulcers, or lumps in the mucosa, tongue,
mouth, or neck.
• Conduct an effective plan of management for a patient with acute mouth
problems:
Outline indications for antibiotic treatment and choice of antibiotics.
Counsel patients about the relationship between plaque and gingivitis
(as well as prophylaxis).
Submandibular duct calculi palpable blmsnually
Resected salivary gland and calculi
273
067 Murmur I Extra Heart Sounds
067A Systolic Murmur
Overview
Systolic murmurs are quite common , frequently 'innocent' flow murmurs. Good clinical
examination techniques are required to differentiate the different cardiac lesions which
give rise to systolic murmurs. The most common pathological lesions are mitral
regurgitation , aortic stenosis and tricuspid regurgitation .
Causes
11) Mitral regurgitation
a) Leaflet
0 Rheumatic fever
0 Collagen diseases (systemic lupus erythematosus (SLE),
scleroderma)
0 Connective tissue diseases (Marfan syndrome I congen ital I mitral
valve prolapse)
0 Endocarditis
0 Hypertrophic cardiomyopathy
b) Chordae tendinae
0 Rupture (myocardial infarction (MI))
0 Mitral valve prolapse
0 Endocarditis
0 Rheumatic fever
0 Trauma
c) Papillary muscle
0 Dysfunction (ischaemia/infarct, aneurysm, dilated cardiomyopathy)
0 Rupture (infarction, trauma)
d) Mitral annulus
0 Calcification (rheumatic fever, chronic renal failure)
0 Dilatation (dilated cardiomyopathy)
I2) Aortic stenosis

a) Leaflet disease
0 Unicuspid, bicuspid (congenital), tricuspid
0 Rheumatic fever
0 Degenerative
b) Sub-valvular disease (hypertrophic cardiomyopathy)
c) Supra-valvular disease (aortic narrowing)
274
I 3) Tricuspid regurgitation
a) Dilatation of right ventricle I tricuspid annulus
0 Right ventricular myocardium (infarction, dilated cardiomyopathy)
0 Pulmonary hypertension I right ventricular dilatation
• Congestive heart failure
• Mitral stenosis/regurgitation
• Primary pulmonary disease (secondary pulmonary hypertension)
• Primary pulmonary hypertension
• Left to right shunt I Eisenmenger syndrome
• Pulmonary valve stenosis
b) Valve abnormality (rheumatic fever, endocarditis especially
secondary to intravenous drug abuse, Ebstein anomaly, carcinoid
syndrome)
I 4) Pulmonary stenosis
Pulmonary stenosis
I 5) Ventricular septal defect (VSD)
Key Objectives
• Determine whether the systolic murmur is innocent or pathologic.
• Determine aetiology of the murmur in the setting of clinical presentation,
the patient's cardiovascular reserve, the clinical examination findings and
evidence obtained from the electrocardiogram (EGG), chest X-ray and
echocardiogram.
• Determine the need for specialist referral and intervention.
• Select patients in need of prophylaxis for bacterial endocarditis.
275
Determine the origin of the murmur.
Define associated murmurs and evidence of structural cardiac
disorders.
Determine whether heart failure is present, and whether left-sided,
right-sided , or both.
Determine whether the heart rhythm is abnormal.
Diagnose abnormal heart rhythm by means of clinical findings and
ECG.
Select diagnostic imaging for further investigation of the systolic
murmur.
• Conduct an effective plan of management for a patient with a systolic
murmur:
Counsel and educate the patient concerning possible need for
endocarditis prophylaxis.
Outline management of heart failure, including side-effects of
prescribed medications.
Discuss the need for anticoagulants in patients with atrial fibrillation .
278
0678 Diastolic Murmur
Overview
A cardiac diastolic murmur is almost always indicative of cardiac pathology. The most
common causes are aortic regurgitation and mitral stenosis. These can usually be
differentiated using good clinical examination skills.
Causal Conditions
1) Aortic regurgitation
a) Leaflet abnormality
0 Bicuspid aortic valve (congenital: usually associated with aortic
stenosis)
0 Endocarditis
0 Rheumatic fever
0 Rheumatoid arthritis (RA), ankylosing spondylitis
0 Trauma
b) Aortic root and ascending aorta
0 Hypertension
0 Marfan syndrome
0 Aortic valve replacement (artificial valve, allograft, xenograft)
0 Dissecting aneurysm
0 Reiter syndrome
0 Ankylosing spondylitis
0 Aortitis (syphilis)
277
I
2) Pulmonary regurgitation
I
3) Mitral stenosis
0 Rheumatic fever
0 Congenital
0 Collagen vascular disease (systemic lupus erythematosus (SLE), RA)
0 Carcinoid syndrome
I 4) Tricuspid stenosis
Key Objectives
• Determine the aetiology of the murmur in the setting of the clinical
presentation, the patient's cardiovascular reserve, the clinical examination
findings and evidence obtained from the electrocardiogram (ECG), chest
X-ray and echocardiogram.
• Determine the need for specialist referral and intervention.
• Select patients in need of prophylaxis for bacterial endocarditis.
Determine the origin of the murmur.
Define associated murmurs and evidence of structural cardiac
disorders.
Determine whether heart failure is present, and whether left-sided,
right-sided , or both.
Determine whether the heart rhythm is abnormal.
Diagnose abnormal heart rhythm by means of clinical findings and
ECG.
Select diagnostic imaging for further investigation of the diastolic
murmur.
• Conduct an effective plan of management for a patient with a diastolic
murmur:
Counsel and educate the patient concerning possible need for
endocarditis prophylaxis.
Outline management of heart failure, including side-effects of
prescribed medications.
Discuss the need for anticoagulants in patients with atrial fibrillation .
278
067C Heart Sounds, Pathological
Overview
Pathological heart sounds are clues to underlying heart disease.
Causes
1) Heart sound 1 (HS1)- mitral valve

a) Loud (mitral stenosis, hyperthyroidism, short PR interval)
b) Soft (mitral regurgitation, long PR interval, chronic obstructive lung
disease, pericardia! effusion)
2) Heart sound 2 (HS2) - aortic and pulmonary components

a) Loud (systemic hypertension, pulmonary hypertension, increased
pulmonary flow)
b) Soft (hypotension, left heart failure, aortic valve stenosis, pericardia!
effusion)
c) No split (Eisenmenger syndrome, severe pulmonary embolus,
pulmonary valve stenosis)
I 3) Altered splitting of heart sounds

a) Increased splitting of HS2
0 Delayed pulmonary valve closure (pulmonary embolus, pulmonary
hypertension, left-right shunt, right bundle branch block (RBBB)
0 Early aortic closure (mitral regurgitation , ventricular septal defect
(VSD))
b) Fixed split (atrial septal defect (ASD))
c) Paradoxical split (left bundle branch block (LBBB), hypertension, left
ventricular outflow obstruction)
I 4) Heart sounds 3 and 4

a) Physiological (young subjects)
b) Third heart sound (dilated ventricle with volume overload, left or right
heart failure, mitral/tricuspid regurgitation)
c) Fourth heart sound (hypertension, heart failure, hypertrophic
cardiomyopathy, aortic stenosis)
279
I 5) Extra heart sound and clicks
a) Ejection sounds (early systolic)- hypertension, aortic and pulmonary
stenosis
b) Opening sounds (early diastolic)- mitral stenosis, tricuspid stenosis
c) Clicks (midsystolic)- mitral valve prolapse
d) Pericardia! knock (pericardia! effusion)
e) Prosthetic valve sounds
Key Objective
• Interpret the origin of heart sounds.
• Through efficient, focused, data gathering:
Determine whether underlying heart disease is present and how the
heart sounds help to define this.
Select common investigative tools such as chest X-ray,
electrocardiogram (ECG), and echocardiography to assist with
diagnosis and understand principles of interpretations of these tests.
• Conduct an effective plan of management for a patient with pathological
heart sounds:
280
068 Neck or Facial Mass I Goitre I Thyroid Disease
Overview
Neck masses may come to clinical attention when noted by the patient as a presenting
symptom, or as an incidental finding during routine physical examination or during a
diagnostic imaging procedure. The most common causes of neck swelling are lymph
node and thyroid gland swellings. Aspiration cytology of focal neck masses is often
helpful in diagnosis of the cause.
Causes
1) Cervical lymph node swellings
a) Associated with overt or occult neoplastic or inflammatory primary
lesions of head and neck
b) Associated with extracervical primary lesions (lung, abdomen, testis)
c) Associated with general lymphadenopathy
12) Thyroid swellings (goitre)

a) Uniform smooth diffuse enlargement (physiologic goitre, Graves
disease)
b) Multinodular enlargement (multinodular goitre)
c) Uninodular (dominant nodule in multinodular goitre, or true solitary
nodule)
Pemberton sign - retrostemal goitre
'Cold' nodule right thyroid

lob8
281
I3) Salivary gland swelling
a) Neoplasm (pleomorphic adenoma, adenolymphoma, etc.)
b) Obstructions (stone)
c) Inflammations (acute or chronic)
Enlarged submandibular salivary

land
14) Embryologic remnants

a) Branchial cyst or fistula
b) Thyroglossa l cyst
c) Lymphoepithelial cyst
Branchial cyst Thyroglossal cyst - moves with tongue
Is) Vascular I Neuroendocrine

a) Carotid body tumour (chemodectoma)
6) Musculoskeletal (sternomastoid tumour, cervical rib)
7) Subjective (normal structure presenting as lump)

a) Normal lymph node, greater cornu hyoid , laryngeal structures,
cervical vertebrae transverse processes
Key Objectives
• Identify likely site of origin and diagnostic significance of neck or facial
lumps by history-taking and careful physical examination.
• Determine the most appropriate investigations required to confi rm
diagnosis.
282
Determine whether the lesion is of rapid onset or insidious.
Determine the presence of hyperthyroidism (including findings typical
of Graves disease) or hypothyroidism.
Perform examination of the thyroid gland, cervical lymph nodes,
salivary glands and other neck and facial structures.
Discuss the utility of thyroid stimulating hormone (TSH) determination
for screening patients suspected of thyroid abnormalities.
Select other thyroid function studies if TSH is abnormal, and outline
their utility.
In a patient with a thyroid nodule, discuss the use of fine needle
aspiration cytology (FNAC) and high-resolution thyroid
ultrasonography.
• Conduct an effective plan of management for a patient with a neck mass
due to goitre/thyroid disease:
Outline a management plan for hyperthyroidism, hypothyroidism,
thyroiditis, and thyroid nodule.
Discuss control of symptoms of hyperthyroidism; discuss advantages
and disadvantages of anti-thyroid drugs and radioactive iodine.
Discuss types of thyroid cancer and their various presentations.
• Discuss diagnosis and management of a patient presenting with clinical
abnormalities of thyroid function without a neck swelling.
• Develop an algorithm for a patient presenting with a neck lump believed
clinically to be a focal cervical node swelling.
• Develop diagnostic and management plans for a patient with generalised
enlargement of cervical lymph nodes.
• Develop diagnostic and management plans for a patient presenting with a
swelling involving left supraclavicular lymph nodes.
focal lymph node swelling in whom FNAC has revealed:
Metastatic adenocarcinoma.
Metastatic squamous cell carcinoma (SCC).
Hodgkin lymphoma.
salivary gland swelling.
• Select patients in need of specialised care.
283
069 Numbness and Tingling
Overview
Disordered sensation may be alarming and highly intrusive. The clinician requires a
framework of knowledge in order to assess abnormal sensation, consider the likely
site of origin, and recognise the implications.
Causes
1) Mononeuropathy
a) Compression from nerve entrapment syndromes, e.g. carpal tunnel
syndrome, ulnar neuropathy
b) Radiculopathy (intervertebral disc lesion, foramina! encroachment)
2) Polyneuropathy (diabetes mellitus, alcoholism, renal failure,

polyarteritis nodosa, systemic lupus erythematosus (SLE),
systemic sclerosis, sarcoidosis, rheumatoid arthritis (RA), AIDS,
leprosy)
3) Spinal cord lesion (cord tumour, infarction, multiple sclerosis,

syringomyelia, vitamin 8 12 deficiency)
4) Brain stem lesion (neoplasm, vascular lesion, demyelinating

lesion)
5) Cerebral hemisphere lesion (tumour, demyelinating lesion,

stroke)
I 6) Hyperventilation
Key Objective
• Determine whether the sensory complaint is positive, also called
paraesthesia or dysaesthesia (tingling, pins and needles, pricking,
burning, knifelike), or negative, termed hypoaesthesia or anaesthesia
(numbness, diminution or absence of feeling) .
Determine the portion of the neural axis likely to be causing the
symptoms.
Contrast peripheral neuropathies, spinal cord or brain stem
dysaesthesia from cortical sensory dysfunction.
Recognise that only negative symptoms or hypoaesthesia may be
detectable on physical examination.
Differentiate between possible causes of the lesion.
284
Select initial laboratory investigations including such tests as nerve
conduction I electromyelography (EMG) and serum vitamin 8 12 levels.
Select patients in need of specialised care for further investigation.
• Conduct an effective plan of management for a patient with numbness and
tingling:
Outline initial management for mononeuropathy.
Z85
070 Pain
(See also #089 Regional Pain)
Overview
Because pain is understood to be a signal of disease, it is the most common symptom
that brings a patient to a clinician's attention. Pain is an unpleasant somatic sensation,
but it is also an emotion. Although CQOtml of P.~L11 .~Jlc;l disco.mfort is a crucial endpoint
of medical care, the degree. of analgesia provided is often inadequate. All clinicians
should be competent to recognise the development and progression of pain, and to
develop strategies for its control.
Causes
1) Face pain (trigeminal neuralgia)
2) Back pain
3) Pain in the cancer patient
4) Pain in the postoperative patient
5) Somatic pain (burn, arthritis, bone metastasis)
6) Visceral pain (intestinal colic, renal 'colic', cancer of pancreas)
7) Neurologic pain (herniated intervertebral disc)
Key Objectives
• State that the ideal treatment for any pain is to remove the cause.
• Because some conditions are so painful that rapid and effective analgesia
is essential (e.g. in first aid, after injury, and after surgery), and in some
conditions it is not possible to remove the cause (e.g. metastatic cancer) ,
demonstrate familiarity with the use of analgesic medications as a first line
of treatment in these cases.
• Discuss that depression, uncontrolled pain, the adverse effects of opioids,
and fear of pain may precipitate suicidal thoughts or requests for aid in
dying.
Determine the most likely cause of the pain (clinical features and use of
provocative manoeuvres are key) .
Because depression is the most common emotional diSt!Jrbance in
patients with chronic pain, elicit evidence of depression.
286
Select laboratory investigations to identify cause of pain if required .
Select patients in need of specialised care for further investigation.
• Conduct an effective plan of management for a patient with acute or
chronic pain:
Categorise and contrast drugs for relief of pain (non-narcotic
analgesics, narcotic analgesi€s, anticonvulsants and anti-arrhythmics,
tricyclic antidepressants, antispasmodics and steroids).
Discuss the use of combinations of medications.
Outline a multidisciplinary approach which utilises medications,
counselling, physical therapy, nerve block, surgery, etc.
Since pain also adds to the discomfort of those caring for the patient
with chronic pain, counsel caregivers.
Select patients in need of referral to a pain clinic or pain specialist.
287
070 Pain
070A Somatic Complaints I Somatoform Disorders
Overview
Non-specific somatic symptoms with no immediate organic explanation frequently
present in primary care. Most are brief but some are persistent and result in repeated
consultations. Somatisation implies the presentation of emotional distress as physical
or bodily symptoms, which mask the underlying anxiety or mood disorder. These
medically unexplained symptoms reflect patients' cog nitive concerns and attributions
about illness in general or about specific con ditio ns, at either a conscious or
unconscious level. Patients' interpretation of bodily sensations may be influenced by
their medical experience and beliefs, their social circumstances and their personality.
Somatoform disorder is the general term to cover all of the different categories of
medically unexplained symptoms.
Causes
t) Acute transient somatic symptoms in response to stress
2) Subacute somatic symptoms in patients with depression or

panic disorder
3) Chronic or recurrent somatic symptoms

a) Somatisation disorder
b) Hypochondriasis
c) Conversion disorder I Dissociative disorder
d) Body dysmorphic disorder
e) Somatoform pain disorder
f) Factitious disorder
g) Malingering
Key Objective
• Differentiate various symptoms such as chest pain, palpitations, dyspnoea,
abdominal pain, etc. which are due to an affective disorder or panic/
anxiety, from similar symptoms due to organic causes.
Elicit history about current life stresses (separation, death, substance
abuse), avoidance patterns or panic attacks, evidence of somatisation
since adolescence, family history of somatisation.
Determine whether there was sexual abuse, physical abuse, emotional
neglect.
288
Select patients for limited laboratory testing, to exclude organic causes.
• Conduct an effective plan of management for a patient with somatic
complaints:
Outline initial management including education about anxiety,
supportive psychotherapy for life stressors, instruction in relaxation
techniques.
Discuss medications available for treatment of somatic complaints I
panic disorder.
289
071 Painful Limb
071A Pain in the Upper Extremities
(See also #089E Shoulder Pai n and #089F Hand/Wrist/Elbow Pain)
Overview
After backache, upper extremity pain is the next most common type of musculoskeletal
pain.
Causes
1) Trauma /Inflammation
a) Torsion, contusion, fracture, dislocation
b) Tendinitis, bursitis, arthritis
c) Frozen shoulder /Traumatised joints
I 2) Nerve impingement
a) Carpal tunnel
b) Cervical spondylosis I Disc herniation
c) Neuritis
d) Tumours
I 3) Degenerative I Rheumatic
a) Arthritis
b) 'Fibromyalgia'
c) Renal osteodystrophy (pseudogout)
Longhead bleeps tendon rupture - re/sxedlcontracted
I 4) Vascular
a) Arterial thromboembolism
b) Raynaud phenomenon
290
Gangrene fingers - vasculitis Pancoast tumour
c) Venous thrombosis
d) Lymphoedema
e) Thoracic outlet syndrome
5) Musculoligamentous (e.g. rotator cuff and other tendon tears

and ruptures, myositis ossificans)
6) Referred
a) Myocardial ischaemia
b) Gallbladder disorders / Subphrenic abscess
c) Apical lung tumour (Pancoast syndrome)
Key Objective
• Demonstrate a careful physical examination with implementation of
specific manoeuvres for diagnosis, since most cases can be diagnosed
without imaging.
Differentiate between various causes of upper extremity pain.
If necessary, select diagnostic imaging and laboratory investigation.
• Conduct an effective plan of management for a patient with pain in the
upper extremities:
Outline a plan of management for various types of upper extremity
pain.
291
071 Painful Limb
071 B Pain in the Lower Extremities
(See also #061 Limp 1 Pain in Lower Extremity in Children)
Overview
The most common cause of leg pain is muscular or ligamentous strain , seen with
increasing frequency with the current interest in physical activity.
Causes
1) Articular (degenerative joint disease)
a) Hip (degenerative joint disease)
b) Knee (degenerative joint disease, gout)
c) Ankle
d) Foot/Toes (gout)
I 2) Non-articular
a) Musculoligamentous (exercise, trauma)
b) Vascular (thrombo-phlebitis, arterial insufficiency, varicose veins)
c) Neurologic (lumbar disc disease, spinal stenosis)
Gangrene foot
292
Key Objectives
• Determine whether the pain is articular (hip, knee , ankle) or non-articular
(muscular, vascular, neurologic) and whether related to exertion or not.
• Recognise that degenerative joint disease and arterial insufficiency
frequently co-exist.
Differentiate between different causes of lower extremity pain by
eliciting essential information (e.g. precipitating events) and
manoeuvres which reproduce the pain.
Perform examination of lower limb including observation of gait and
posture, examination and determination of range of motion of joints,
measurement of calves and thighs, and palpation of peripheral
arteries.
List indications for radiographic, magnetic resonance imaging (MAl),
and arthroscopic examination.
• Conduct an effective plan of management for a patient with pain in the
lower extremities:
Outline a multidisciplinary plan of management for lower extremity pain
caused by degenerative joint disease.
Outline a multidisciplinary plan for prevention of peripheral vascular
disease.
Outline a plan of management for exercise-induced injuries which
makes possible the return to physical activity.
293
071 Painful Limb
071 C Painful Lower Limb - Varicose Veins
Overview
Varicose veins are dilated. tortuou s, elongated veins in the lower limb. They may
present as concern with the cosmetic appearance of the visible venous swellings. or
as a source of local chronic discomfort worse on standing and eased by recumbe~cl:'.
Acute symptoms result from localised acute thrombosis in su perficial veins (superficial
thrombophlebitis) causing a painful palpable subcutaneous cord. Deep venous
thrombosis (DVT) may complicate superficial varices or arise independently (see
#0348 Unilateral Limb Oedema (Swollen Limb)). In the post-thrombotic syndrome,
leg ulceration follows ~hronic deep venous insufficiency. Significant risk factors
associated with 'primary' vascular veins are the female sex. pregnancy and multiparity,
and a family history.
Causes
1) 'Primary' varicose veins of lower limb- cause unknown

Often associated with female gender, systemic hormonal eHects. pregnancies. familial
influences , iliac (left) vein com pression ; or to primary valvu lar incompetence in
superficial veins and in the commu nications between deep and superficial venous
system.
2) 'Secondary' varicose veins of lower limb

Superficial varices secondary to deep venous obstruction or incompetence.
arteriovenous fistu lae. or compression from pelvic mass.
Chronic deep venous

Varicose veins - ssphenofemoral
incompetence
294
3) Miscellaneous causes of dilated superficial veins
a) Distal venous obstruction (e.g. retrosternal goitre)
b) Diversionary anastomotic channels (e.g. obstructed superior or
inferior vena cava, effects of portal hypertension)
c) Arteriovenous malformations
Key Objectives
• Differentiate between uncomplicated, primary superficial varices and those
associated with chronic deep venous insufficiency.
• Understand the principles of assessment of a patient presenting with
symptomatic varicose veins.
Appreciate the general anatomy and physiopathology of the superficial
and deep venous systems of the leg, and their interrelationships during
standing and activity.
Recognise the common sites of communication between superficial
and deep venous systems; and the principles and practice of tests for
valvular incompetence.
Ability to answer the diagnostic questions:
Are definite superficial varices present, and do they involve the long
or short saphenous system or both?
* Are signs of vascular incompetence, particularly saphenofemoral
incompetence, present; and are there signs of incompetent
communicating or perforating veins below groin level?
* Are the deep veins normal or is there evidence of deep venous
circulatory insufficiency?
• Conduct an effective plan of management for a patient presenting with
symptomatic varicose veins:
Outline noninterventional methods of management.
Outline indications and principles of sclerotherapy.
Outline indications for surgery and select patients for onward referral
and further investigation.
295
072 Palpitations (Abnormal Electrocardiogram (ECG) I
Arrhythmia)
Overview
The symptom of palpitations describes an abnormal subjective awareness of the
heart beat. Patients can usually distinguish between occasional, intermittent or
continuous bouts of palpitations and whether they are regular or irregular. In this
regard, asking the patient to tap out the beats on a table can often clarify the important
features. Palpitations are commonly associated with anxiety and vasodilatational states
but may indicate a more serious cardiac arrhythmia where there are usually associated
symptoms (sweating, breathlessness, dizziness, fainting, chest pain) which can give
important clues to the diagnosis. The definitive diagnosis requires a clinical assessment
and/or electrocardiogram (EGG) during a bout of palpitations.
Causes
t) Sinus rhythm
a) Vasodilatation I Sinus tachycardia (exercise, stress, fever, pregnancy,
menopausal state, drugs)
b) Anxiety
c) Ectopic beats
j2) Atrial tachyarrhythmias

a) Atrial premature complexes
b) Atrial flutter and fibrillation
Idiopathic (lone fibrillator)
0 lschaemic heart disease
0 Hypertensive heart disease
0 Valvular heart disease
0 Thyrotoxicosis
0 Cardiomyopathy {alcoholic, idiopathic, viral)
0 Electrolyte disorders
0 Drugs
-
~
.. .
-.. ... ::;:::
r=:::: :-:-:- ..
- .,....,
---
~--= f;::::
- - -- II
~
1::::
II
1-·~ ...... ~ .. ..
Atrial flutter
296
I 3) Supraventricular tachycardia
a) Paroxysmal supraventricular tachycardia
b) Wolff-Parkinson-White syndrome (WPW) I Concealed bypass tract
c) Multifocal atrial tachycardia
I 4) Ventricular tachyarrhythmias I
a) Premature ventricular ectopics
b) Ventricular tachycardia
0 Sustained
0 Non-sustained
Key Objectives
• Select patients in need of urgent treatment.
• Differentiate palpitations due to intrinsic heart disease from those that are
a manifestation of anxiety, exercise, or other systemic disease (differentiate
from sinus tachycardia).
• Understand the indications for the use of drugs and when there are
contraindications to particular drugs because of their pro-arrhythmic
potential.
• Know when and how to use anticoagulant drugs in the patient with atrial
fibrillation .
Contrast benign palpitations to those associated with serious disease.
Diagnose major cardiac arrhythmias.
Differentiate between causes of palpitations.
Elicit and interpret signs and symptoms which indicate that a cardiac
arrhythmia requires immediate treatment.
Select and interpret appropriate investigations for patients presenting
with palpitations, including cardiography and Holter monitoring.
• Conduct an effective plan of management for a patient with palpitations:
Outline initial management for the patient with an abnormal heart
rhythm .
Select the patients in need of specialised care and/or consultation,
including those with a benign or unknown aetiology.
Describe the indications for anticoagulant and/or anti-platelet therapy
for patients with arrhythmias and perform initial and long term
management.
297
073 Panic and Anxiety
Overview
The anxiety disorders are characterised by excessive and persistent worry, anxiety
or fear, and avoidant or controlling behaviours and phenomena, accompanied by
physical symptoms of hyperarousal and autonomic hyper-reactivity. They occur
commonly, and may present acutely (for example panic attacks) or with chronic
impairment (for example , generalised anxiety disorder) . Presentation with
predominantly somatic symptoms, either a single compla int (e.g. chest pain ,
neurological deficit) or a large number of multisystem symptoms, through the process
of somatisation, is frequent. The anxiety disorders are:
0 Generalised anxiety disorder: enduring six months or more of excessive worry
and anxiety, with muscle tension and physical indicators of hyperarousal, such as
sleep and concentration disturbance, fatigue.
0 Panic disorder, with or without agoraphobia: sudden anxiety attacks; fear of
collapse, loss of control, or death; and hyperarousal, especially hyperventilation
and its sequelae; with situational avoidance.
0 Phobias (specific, agoraphobia, and social): excessive, unreasonable fear of
specific situation, with avoidance, or extreme sensitivity and anxiety if endured.
0 Post-traumatic stress disorder: exposure to extreme, threatening event and
subsequent persistent hyperarousal, intrusive re-experiences, and avoidance of
the trigger and allied events.
0 Obsessive-compulsive disorder: recurrent and irrepressible thoughts, images
or impulses, accompanied by anxiety symptoms, and repetitive driven habits or
rituals to reduce distress or some anticipated dread.
Causes
1) Physical causes of anxiety
a) Cardiovascular (angina, arrhythmias)
b) Drugs (caffeine, amphetamines, cocaine)
c) Metabolic I Endocrine (thyroid, phaeochromocytoma)
d) Neurological (encephalopathy, temporal lobe seizure, dementia)
e) Respiratory (asthma, emboli, oedema)
2) Non-physical conditions causing anxiety

a) Primary anxiety disorders (see Overview)
b) Other psychiatric conditions- depression, substance abuse
disorders, schizophrenia
298
Key Objectives
• Identify the presence of a primary anxiety disorder and its type.
• Differentiate from secondary anxiety arising from other psychiatric
conditions, physical causes or drugs, and from realistic anxiety arising
from an environmental threat.
Elicit a history of excessive anxiety, fear or worry along with other
symptoms specific to the particular anxiety disorder.
Determine the level of social, occupational and general functional
disability.
• Interpret those clinical and laboratory findings key to the diagnostic
process.
• Implement an appropriate management plan for the particular anxiety
disorder and level of disability:
Education about the condition, causes and symptom manifestations.
General anxiety management including relaxation methods,
hyperventilation control, and graduated exposure to trigger situations.
Specific intervention with problem-solving techniques and cognitive
behavioural therapy, or specialist referral.
Selected drug therapy such as antidepressants.
299
074 Papanicolaou (Pap) Smear I Screening I Prevention
Overview
Any female patient who visits a clinician's office should have current screening
guidelines applied and if appropriate, a Papanicolaou (Pap) smear should be
recommended.
Causes
11) Normal
I 2) Abnormal
a) Benign atypia
0 Atypical glandular cells of uncertain significance (AGUS)
0 Atypical squamous cells of uncertain significance (ASCUS)
0 Infection
b) Human papilloma virus (HPV)
c) Mild/Severe dysplasia - cervical intra-epithelial neoplasia (CIN)
0 CIN 1 - also called mild dysplasia
0 CIN 2- also called moderate dysplasia
0 CIN 3- also called carcinoma-in-situ
d) Invasive carcinoma (micro)
I 3) False positive or negative smears
Key Objective
• Select patients in need of referral for further investigation including
colposcopy and target biopsy after the report of a Pap smear becomes
available.
Determine whether the patient is at high risk for developing cervical
dysplasia or invasive disease.
List situations which increase the index of suspicion for cervical
dysplasia.
Describe how to obtain a Pap smear.
Select additional investigation if appropriate.
300
• Conduct an effective plan of management for a patient with abnormal Pap
smear:
List recommendations for prevention of cervical dysplasia I cervical
cancer and identify health promotion strategies for young sexually
active women.
Discuss the role of regular cervical cytology in the prevention of
invasive disease.
Outline methods of treatment for pre-invasive disease of the cervix and
list possible complications.
Discuss the association of HPV infection with CIN neoplasia and
invasive cancer (including the most common HPV sub-types
associated with progression to invasive cancer).
Discuss the specificity and sensitivity of Pap smear test, and factors
leading to a false positive or negative test.
301
075 Pelvic Mass
Overview
Pelvic masses are common in cl inical practice and need to be investigated to find the
cause.
Causes
1) Gynaecologic
a) Ovary
0 Functional cysts (follicular, corpus lutein cysts, theca lutein cysts)
0 Hyperplastic (polycystic ovary, endometriotic cyst)
0 Neoplastic
• Serous cystadenoma I Carcinoma
• Mucinous cystadenoma I Carcinoma
• Thecomas I Granulosa cell tumours
• Fibromas
• Germ cell tumours (cystic teratoma, teratoma, gonadoblastoma,
dysgerminoma)
b) Tube (salpinx)
0 Ectopic pregnancy
0 Inflammation (including hydrosalpinx/pyosalpinx), cysts
(mesonephric, paramesonephric)
c) Uterus
0 Pregnancy
0 Haematometra I Pyometra
0 Leiomyoma/Adenomyoma
0 Sarcoma
2) Non~ynaecologic (bowel, bladder, other)
302
Key Objectives
• Determine whether the patient may be pregnant.
• Determine whether the mass is gynaecologic, and whether the origin is the
ovary, tube, or uterus.
Elicit a history including menstrual, fertility, and obstetrical history,
sexual activity, and associated symptoms.
Perform abdominal and pelvic examination including speculum
examination.
Describe features suggestive of androgenisation in the reproductive
age and oestrogenisation in prepubertal age group.
List blood tumour markers if malignancy is suspected; pregnancy test
and/or cultures if indicated.
Select diagnostic imaging appropriate for mass, or endometrial biopsy
if indicated.
• Conduct an effective plan of management for a patient with a pelvic mass:
Outline management of functional cysts.
Outline management of tubo-ovarian abscess.
Counsel patients with leiomyoma and outline medical management.
303
076 Pelvic Pain
Overview
Many hours each year are lost from school and work due to pelvic pain. Successful
treatment requires a correct diagnosis. Once the diagnosis is established, specific
and usually successful treatment may be instituted.
Causes
1) Pregnancy-t""elated
a) Ectopic pregnancy
b) Aborting pregnancy
c) Gynaecological conditions in pregnancy - complicated ovarian cysts,
red degeneration of a leiomyoma
d) Molar pregnancy
I 2)" Gynaecological
a) Mittelschmerz
b) Torsion (e.g. ovarian)
c) Endometriosis
d) Bleeding into a pelvic mass I Ruptured pelvic mass
e) Infection (e.g. salpingitis)
f) Dyspareunia
3) Non-gynaecological (gastrointestinal, renal, musculoskeletal)
Key Objective
• Determine whether the pain is acute or chronic, whether pregnancy is
likely, and stabilise the patient whose pain is acute and life-threatening.
Elicit a history including menstrual, fertility, and obstetrical history,
sexual activity, and associated symptoms.
Determine whether the patient's condition is haemodynamically stable
and whether a candidate for possible emergency surgery.
Perform abdominal and pelvic examinations including speculum
examination.
304
List guidelines for ultrasound in pregnancy; obtain pregnancy test.
Select appropriate diagnostic imaging; list indications for laparoscopy.
• Conduct an effective plan of management for a patient with pelvic pain:
List indications for dilatation and curettage, laparoscopy, and
laparotomy for aborting pregnancy or ectopic pregnancy including
impact on future fertility.
Outline initial management of endometriosis.
Outline management of acute salpingitis.
Counsel for the purpose of preventing sexually transmitted diseases
(STDs).
Counsel and outline management of patients with chronic pelvic pain
associated with psycho-emotional factors.
Outline management of dyspareunia.
305
077 Periodic Health Examination I Growth and
Development
Overview
Periodically, patients visit clinicians' offices not because they are unwell, but because
they want a 'check-up'. The periodic health examination is considered an opportunity
to relate to an asymptomatic patient for the purpose of case finding and screening for
undetected disease and risky behaviour. It is also an opportunity for health promotion
and disease prevention, particularly in regard to immunisation, tobacco and alcohol
abuse, and monitoring growth and weight.
Causal Conditions to be Considered

1) Infant and toddler less than 3 years (e.g. delayed growth,
development, abuse/neglect)
2) Child 3-12 years (visual/hearing deficit, accidents, development,

abuse/neglect)
3) Youth 13-24 years (motor vehicle accident (MVA), substance

abuse, sexually transmitted diseases (STDs), sedentary)
a) Female (rubella immunisation, contraception)
b) Male (contraception)
4) Adult 25-44 years (substance abuse, eating disorders, family

violence)
a) Female (cervical cancer, hypertension)
b) Male (hypertension, elevated cholesterol, MVA)
5) Middle age 45-64 years (lung cancer, colon cancer, skin cancer,
obesity)
a) Female (osteoporosis, breast cancer)
b) Male (prostate cancer, ischaemic heart disease)
c) Hypercalcaemia - both sexes
6) Seniors older than 64 years (elder abuse, falls, drug-related

morbidity, nutrition, cancer)
Key Objectives
• Determine patient's risks for common gender/age specific conditions.
• Elicit information about ethnic, family, socio-economic, occupational,
lifestyle characteristics that are known to be at high-risk for a particular
condition.
306
In an infant, toddler, or child, elicit information about risk factors at
conception, pregnancy, and birth, familial factors, and existing signs of
illness or environmental risk factors (missed immunisation, diet,
passive smoke inhalation, skin protection).
Determine height, weight, head ci rcumference, medical status, and
developmental milestones.
For a youth, elicit information about nutrition, physical activity, drug use,
sexual/social/peer activities, emotional concerns, communication with
parents.
In adults, elicit information about lifestyle patterns, psychological,
social, and physical functioning, symptoms of any illness, and
situational factors affecting mood.
In seniors, elicit information about past illness, lifestyle factors, mental
function, drug use, physical and social activity, emotional concerns,
social relations and support systems.
Select investigation specific to age and gender concerns.
• Conduct an effective plan of management for a patient who is well and
without disease, well and with disease, not well and with disease, not well
and without disease:
Communicate regarding disease and accident prevention; encourage
patient control over health.
Outline interventions that would reduce risk for an existing condition
detected.
For a frequently encountered risk factor (e.g. colon cancer), outline
interventions that would reduce the risk for the condition.
Remember when considering major interventions that it is difficult to
make an asymptomatic patient feel better.
307
077 Periodic Health Examination 1 Growth and
Development
077A Newborn Assessment/Nutrition
Overview
Primary care clinicians, paediatricians and obstetricians play vital roles in identifying
children at risk for developmental disabilities. Parents require direction and
reassurance regarding the health status of their newborn infant. In most cases, parental
concerns regarding the child's language development, articulation, fine motor skills,
and global development are likely to be associated with true developmental delays.
Parental concerns with personal-social skills are associated with developmental delays
in some cases.
Causes
l1) Developmental surveillance
2) Nutrition (breastfeeding, bottlefeeding, solid foods)
I 3) Well-newborn care
Key Objectives
• Determine development through ongoing monitoring because new
circumstances may interfere (e.g. medical illness, family disruption) or
because, as children develop. new categories of skills are gained (e.g.
language delays cannot be detected before 18-24 months).
• Provide anticipatory guidance to parents in order to prevent unnecessary
demands from healthcare providers.
• Through efficient, focused. data gathering:
Elicit history of parental concerns regarding the child's development,
risk factors for developmental delays, and attainment of developmental
milestones.
Perform examination of head circumference, congenital anomalies or
dysmorphic features, skin lesions (e.g. cafe-au-fait spots, ash leaf
macules, 'port-wine' naevi) , muscle tone, hearing, vision, and
developmental screening tests.
308
• Conduct an effective plan of management for the newborn:
Counsel parents regarding breastfeeding (maternal drug use during
lactation, maternal nutrition and rest, breastfeeding technique, feeding
frequency and intake), bottlefeeding technique, frequency and intake,
formula types, and introduction of solid food , vitamin requirements and
the indications for dietary supplements; discuss contraindications to
breastfeeding.
Determine the measurements appropriate for normal infant growth and
development.
Counsel parents about skin care, fontanelles, eye colour, strabismus,
teeth, umbilicus, genitalia, urination and defaecation.
309
Development
0778 Infant and Child Immunisation
Overview
Immunisation has reduced or eradicated many infectious diseases and has improved
overall world health. Recommended immunisation schedules are constantly updated
as new vaccines become available.
Causes to be Prevented
1) Poliomyelitis
2) Diphtheria-Tetanus-Pert ussis
3) Measles-Mumps-Rubella
4) Hepatitis B
5) Chicken pox
6) Pneumococcal pneumonia
7) Meningococcal meningitis
8) Influenza
Key Objectives
• Discuss the population health benefits of immunisation programmes.
• State that a lapse in immunisation schedule does not require re-instituting
the initial series, merely correcting the lapse at the next visit.
• Communicate to patients and parents about vaccine benefits and risks.
Obtain an immunisation history on all children and determine whether
the child (or family member) is immunosuppressed or is receiving
immunosuppressive drugs.
Determine whether the child has had splenectomy (also congenital or
functional in sickle cell disease).
310
Test immune status of susceptible children.
• Conduct an effective plan of management which will:
Discuss misconceptions about immunisation contraindications and
actual contraindications.
List possible complications of immunisation.
Discuss immunisation of immuno-compromised children (e.g. with
asplenia, chronic diseases or seizures).
311
Development
077C Preoperative Assessment
Overview
Accurate and thorough evaluation of patients prior to surgery will maximise the chance
of successful outcome. The objectives of such an evaluation include the determination
of risk of the intended procedure to the patient and what measures may be required to
minimise such risks. Pivotal in the process is counselling of the patient (and where
appropriate, family members) with appropriate explanation of the procedure, its benefits
and its risks.
Considerations in Preoperative Assessment
1) Understanding of the procedures - potential risks,

complications and side-effects
2) Preoperative assessment of risk factors and comorbidities

a) Optimal care of recognised diseases I risk factors
b) Identification of unrecognised diseases I risk factors
c) Identification/Management of potential complications
0 Anaesthetic/Postoperative risk
• Myocardial dysfunction
• Autonomic neuropathy (e.g. diabetes mellitus)
• Pulmonary risk (upper abdominal/thoracic surgery, duration
greater than three hours, smoking and/or chronic obstructive lung
disease, PaC02 greater than 45 mm Hg, obesity, etc.)
• Drugs (e.g. anticoagulants, analgesics, psychotropics)
0 Exercise capacity
0 Other
Key Objectives
• Identify factors likely to influence peri-operative and postoperative
morbidity and mortality.
• Identify measures required to reduce morbidity and mortality of surgery.
• Communicate to the patient and the preoperative team the level of risk for
the proposed surgery compared to average risk for the procedure rather
than 'clearing' or 'not clearing' patients for surgery.
312
• Through efficient, focused data gathering; identify potential risks from
history-taking, examination and preoperative investigations:
Elicit evidence of feeling unwell, serious past illnesses and any
medications in previous three months.
Elicit evidence of dyspnoea, cough, wheeze, chest pain on exertion,
ankle oedema.
Obtain history of allergies, previous anaesthetics, problems with
anaesthetics (including in family) ; and in women, their last menstrual
period.
Note history of previous surgery, bleeding tendency, aspirin,
nonsteroidal anti-inflammatory drugs (NSAIDs) or anticoagulant
medication, or previous transfusions.
Select and interpret preoperative laboratory investigations based on
known or clinically suspected diseases or risk factors (e.g. cardiac or
pulmonary disease, diuretic use, diabetes, hypertension) or the age
and sex of the patient.
Identify patient-related and procedure-related risk factors.
Grade surgical and anaesthetic risk according to the American Society
of Anaesthiologists (ASA) classification.
• Conduct an effective plan of management for a patient with illnesses or
risk factors :
Recommend smoking cessation eight weeks preoperatively in
smokers.
Explain why 'routine' preoperative investigations are not indicated.
Discuss postoperative pain control including various analgesics,
epidural analgesia, and intercostal nerve block in patients at risk for
pulmonary complications.
313
Development
0770 Postoperative Patient Evaluation and Care
Overview
Wound care is required after any surgical procedure and any complications of the
healing process need early diagnosis and management. General observational and
nursing care of the surgical patient is equally important. Optimal patient care and
regular systems review can avert potential compl ications or detect and reverse them
at an early stage.
Causes of Potential Postoperative General Complications

1) Wound - delayed wound healing associated with haematoma/
seroma, infection, dehiscence; incisional hernia
Atelectasis - preoperative and postoperative films
2) Airway/Breathing/Chest - atelectasis, aspiration, pneumonia,

postoperative respiratory failure, pulmonary embolism
13) Circulation
a) Haemorrhage
0 Wound - primary, reactionary, secondary; overt or concealed
0 Gastrointestinal haemorrhage - stress ulcer syndrome
b) Shock- haemorrhagic, cardiogenic, obstructive/embolic, septic
c) Cardiac - arrhythmias/arrest, myocardial infarction (MI), cardiac
failure
4) Gastrointestinal - postanaesthetic nausea/vomiting, disturbed

bowel function, bowel obstruction, gastrointestinal haemorrhage,
jaundice, parotitis
5) Urinary - retention, infection, acute renal failure (ARF)
314
6) Integument and vascular access - thrombophlebitis,
extravasation of intravenous solutions, pneumothorax (central
cannulation), incompatible blood transfusion, diathermy burn,
pressure sore
7) Cerebral - delirium: hypoxia; drugs/intoxication/withdrawal;

sleep loss I disorientation; metabolic disturbance; sepsis
8) Fever - atelectasis; focal or systemic sepsis; thrombophlebitis;

deep venous thrombosis (DVT) and thromboembolism; tissue
necrosis I gout I Ml; incompatible blood transfusion; drug allergy
Key Objectives
• Optimally monitor postoperative course by regular wound assay,
observation of vital signs, focused systems review and followup .
• Encourage early return of preoperative functions.
• Achieve early detection and treatment of complications.
• Through efficient, focused data collection, including investigations where
appropriate:
Monitor early postoperative progress, supervise and maintain
uncomplicated postoperative progress.
Check for adequate pain relief; and that vital signs are normal from
nursing observations. Check wound status and fluid balance;
intravenous drip sites and urethral catheter care if present; assess
chest, abdomen, legs for DVT, circulation and temperature at regular
intervals.
Anticipate postoperative pharmaceutical requirements, followup by
surgeon, and by patient's own family doctor to co-ordinate overall
patient care.
Liaise with other health workers including ward and district nursing
staff, paramedical care including: physiotherapy, occupational therapy,
speech pathology, social worker and community service workers as
required.
Communicate with family members, other relatives and friends as
appropriate.
Communicate with patient's doctor verbally and arrange early
transmission of summary of admission, operative and postoperative
details.
Communicate accurately, empathically and at an appropriate level with
patient during early convalescence and prior to discharge and answer
any continuing concerns.
315
Development
077E Work-Related Health Issues
Overview
Doctors will encounter health hazards in their own work place, as well as in the work
place of their patients. These hazards need to be recognised and addressed.
Causes
1) Disability management and work fitness
I2) Public health and surveillance

a) Hazard recognition, evaluation, and control
b) Occupational and environmental injury/illness
c) Underlying medical condition and environment
I 3) Clinical preventive services
Key Objective
• Determine whether the work place or environmental conditions are
potentially hazardous, the impact on the health of the workers, and
recommend preventive strategies.
Elicit history of patient's occupation and possible exposure to toxic or
hazardous environments and identify potential relationship to patient
presentation.
• Conduct an effective plan of management for a patient with work-related
health issues:
Select patients in need of specialised care and provide followup care.
Counsel patients about safety issues and report findings to affected
patients as well as employers (considering medical confidentiality
issues).
316
• Gain an understanding of Australian WorkCover law:
Legal obligations of employers:
. To provide a safe workplace .
• To indemnify employees against work-related injury.
The process of completing and submitting an Australian WorkCover
form when treating patients with work-related injury or illness.
The limits of the indemnity cover provided by WorkCover law in
Australia.
317
Development
077F Health of Special Populations
Overview
The health of groups frequently reflects the influences of health determinants such as
the ones considered in #077G Population and #077H Environment. T he conditions
resulting from these adverse factors do not differ from those considered under the
numbered clinical presentations indicated, but are here re-considered in order to alert
learners to the most common conditions to be considered in these respective groups.
Causal Conditions to be Considered in Individual Population Groups

1) The health of indigenous aboriginal peoples
a) Trauma I Poisoning I Sudden infant death syndrome (SIDS) I Acute
life-threatening event (ALTE)
(see #079 Poisoning, #099 Sudden Infant Death Syndrome (SIDS) ,
(Acute Life-Threatening Event (ALTE)), #1 07 Substance Abuse/Addiction,
#1 08 Suicidal Behaviour/Prevention, #1 13 Trauma/Accidents/Prevention)
'
b) Circulatory diseases (including rheumatic fever)
(see #020 Chest Discomfort, #032 Dyspnoea and/or Cough I Prevention of
Cancers and Chronic Respiratory Diseases, #054 Hypertension, #067
Murmur I Extra Heart Sounds)
c) Neoplasms
(see #016 Bleeding with Defaecation I Acute Lower Gastrointestinal
Bleeding I Melaena I Occult Blood in Stool I Prevention of Cancer, #048
Haematemesis I Melaena, #049 Haematuria, #051 Haemoptysis, #070
Pain, #125 Weight Loss I Eating Disorders I Anorexia I Nutritional Disorders)
d) Diseases of respiratory system
(see #032 Dyspnoea and/or Cough I Prevention of Cancers and Chronic
Respiratory Diseases, #126 Wheezing I Respiratory Difficulty I Stridor)
e) Infection (gastroenteritis, otitis media, infectious hepatitis)
(see #027 Diarrhoea/Constipation, #033 Ear Pain, #040 Fever and Chills
(Adult and Paediatric), #058 Jaundice)
f) Diabetes
(see #053 Hyperglycaemia I Diabetes Mellitus)
g) Skin disorder
(see #101 Skin Blisters - Boils -Comedones- Ulcers, #1 01 A Chronic Leg
Ulcer)
318
I 2) The health of seniors
a) Musculoskeletal (including falls and Injuries)
(see #037 Falls, #059 Joint Pain, Mon-Articular (Acute, Chronic), #060
Joint Pain, Poly-Articular (Acute, Chronic), #089 Regional Pain)
b) Hypertension/Heart diseases
(see #020 Chest Discomfort, #032 Dyspnoea and/or Cough I Prevention of
Cancers and Chronic Respiratory Diseases, #054 Hypertension, #067
Murmur I Extra Heart Sounds)
c) Respiratory diseases
Respiratory Diseases, #126 Wheezing I Respiratory Difficulty I Stridor)
d) Dementia
(see #024 Dementia I Memory Disturbances)
3) The health of children in poverty (single mothers, immigrants)

a) Low birth weight
(see #123 Weight (Low) at Birth I Intra-uterine Growth Aberration)
b) Trauma I Poisoning
(see #079 Poisoning, #113 Trauma/Accidents/Prevention)
c) Mouth problems
(see #066 Mouth Problems)
d) Fever / Infectious diseases
(see #040 Fever and Chills (Adult and Paediatric), #058 Jaundice)
e) Psychiatric problems
(see #065 Mood Disorders, #073 Panic and Anxiety, #078 Personality
Disorders, #107 Substance Abuse/Addiction, #108 Suicidal Behaviour/
Prevention, #11 9 Violence/Aggression and Mental Illness, #125 Weight
Loss I Eating Disorders I Anorexia I Nutritional Disorders)
4) The health of people with disabilities
Key Objective
• When providing a periodic health examination to a person belonging to
one of the above groups, evaluate conditions common to the group and
determine whether evidence exists that the individual has such a
cond ition.
319
Development
077G Population
Overview
Some people are healthy while others are not, for reasons other than biology, genetic
endowment, and the physical environment. The social environment exerts a profound
influence on health , and social stimuli may exert a profound effect on physical
responses.
Causal Determinants of HeaHh

j1) Income and social status
j 2) Social support network
I 3) Education
4) Personal health practices and coping skills
I 5) HeaHhy child development
6) HeaHh services (access and barriers to access)
I 7) Employment and working conditions

(see #077E Work-Related Health Issues)
I 8) Physical environment
(see #077H Environment)
I 9) Biology and genetic endowment
Key Objectives
• Discuss the three levels of disease prevention (primary, secondary, and
tertiary) and strategies for health promotion (e.g. education,
communication/behaviour change, social marketing, healthy public policy,
community development and organisation, community-wide prevention,
and diffusion of innovations).
• Explain that factors such as geographic location, gender, and ethnic origin
•
influence some of the determinants of health, but health status is in turn
influenced by differential allocation and distribution of health service
resources.
320
Identify needs of population with survey information and other sources
in order to select interventions or management strategies for clinical
presentations (e.g. education about seat belts, education about herbal
medications since some weight reduction herbal medications can
cause chronic renal failure) .
Elicit history concerning occupation, education, level or absence of
control, cultural issues, etc. that may have had an impact on presenting
condition .
• Conduct an effective plan of management for patients with conditions
related to determinants of health:
Select population issues better managed by means of health
promotion rather than traditional medical interventions.
321
Development
077H Environment
Overview
Environmental issues are important in medical practice because exposures may be
causally linked to a patient's cl inical presentation, or a patient's reported environmental
exposure may necessitate interventions to prevent futu re illness. Clinician involvement
is important in the promotion of global environmental health.
Exposures to Causal Environmental Pollutants

j 11 Air pollutants
a) Biological
0 Pollen
0 Home exposures (dust mites, cockroaches, etc.)
b) Chemicals
0 Lead
0 Fossil fuel related (e.g. CO, 802 )
0 Indoor air pollutants (e.g. formaldehyde)
0 Secondhand tobacco smoke
c) Physical (energy transfer)
0 Radiation (e.g. ultraviolet (UV) from ozone layer destruction by
chlorofluorocarbons)
0 Electricity
2) Water pollutants (drinking/recreational water)

a) Bacterial
b) Chemical/Industrial
3) Soil pollutants (chemical/industrial)
I4) Food pollutants

a) Biological (toxins/bacteria)
b) Chemical
0 Drugs (antibiotics , hormones)
0 Food preservatives
0 Pesticides
322
Key Objectives
• Describe clinical presentations caused or aggravated by environmental
exposures that are virtually indistinguishable from ones caused by other
conditions (e.g. headache from carbon monoxide poisoning is similar to
tension headache or migraine; asthma).
• In patients whose immediate (e.g. allergic reaction), subacute (e.g.
asthma), or delayed (e.g. pneumoconiosis) presentation may be linked to
environmental exposure, elicit an environmental history and identify
potential sources of problems.
General/Specific Objecthres
Determine whether symptoms are worse at home, work, or at leisure
activities, on weekends or work days and are related to recent or past
exposures (e.g. fumes, dusts, chemicals, radiation).
Determine whether an illness is occurring in an unexpected person
(e.g. lung cancer in a non-smoker) or whether symptoms have
developed without a clear aetiology.
Determine presence of nearby industrial plants, commercial
businesses, or dump sites.
Determine home insulation, heating and cooli ng systems, cleani ng
agents, pesticide use, water supply, water leaks, recent renovations, air
pollution, hobbies, hazardous waste contamination, spills, or other
exposures.
Select and consult labels or Material Safety Data Sheets (MSDS),
poison control centres, consultants, agencies, and other references for
information.
Select consultants (environmental medicine specialists, toxicologists,
governmental agencies, industrial hygienists, etc.) for the purpose of
documenting and quantifying exposure.
Select laboratory tests for the patient to establish exposure or select
investigations to establish the presence of adverse health effects on
target organs (e.g. blood lead levels to assess exposure to lead and
serum creatinine to look for effects on kidney function).
• Conduct an effective plan of management for a patient with possible
environmental exposure:
If evidence supports, or a strong suspicion exists, for a causal
connection between exposure and the cli nical presentation, notify the
appropriate authorities to inspect the site and thereafter to decrease or
eliminate exposure.
323
078 Personality Disorders
Overview
Personality disorders are deeply ingrained , inflexible and persistent maladaptive
behaviours, which have been present since adolescence. These enduring patterns of
behaviour exhibited over a wide variety of social, occupational and relationship contexts
have adverse effects on the individual and on society. Abnormal personalities
predispose to anxiety, mood disorders and alcohol and substance abuse, although
they may co-exist with positive and favourable traits. Abnormal personalities occur in
about five percent of the general population and thus need to be recognised by clinicians.
Causes
1) 'Odd' personality (paranoid, schizoid, schizotypal)
2) 'Dramatic' personalities (borderline, histrionic, narcissistic)
3) 'Anxious' personalities (dependent, avoidant,

obsessive<ompulsive)
I 4) Antisocial personality disorder
5) Others (passive-aggressive, explosive)
I 6) Mixed patterns
Key Objective
• Determine whether the pattern of behaviour exhibited is enduring and
exhibited over a wide variety of social and personality contexts leading to
impairment in social and occupational functioning.
Determine whether the patient is excessively suspicious or jealous,
isolative, aloof or emotionally cool with little need for personal
relationships, or has eccentric ideas or disturbances in thinking and
communication.
Determine whether there is excessive sensitivity or depression,
perfectionism and inflexibility, shyness and withdrawal , or excessive
dependence on others.
Elicit history of lying, truancy, fights, thefts, cruelty, arson, substance
or illegal activity before the age of 15 years; along with a pattern of
manipulation and exploitation of others; impulsivity; a lack of empathy
or remorse; and instability of mood or affect.
Determine whether there is excessively dramatic, flamboyant attention-
seeking, excitable, grandiose and emotional behaviour.
324
• Develop an effective management plan for a patient with a personality
disorder:
Outline differences between supportive therapy; insight-oriented
therapy; cogn itive and behavioural therapy; family or couple therapy
and group therapy.
Identify patients who will need drug and alcohol counsellmg .
Identify patients who will benefit from treatment for anxiety or mood
disorders.
Select and refer patients who will benefit from specialised assessment
and care .
325
079 Poisoning
Overview
Exposures to poisons or drug overdoses account for 5- 10% of emergency department
visits, and greater than 5% of admissions to intensive care units. More than 50% of
these patients are children less than six years of age.
Causes
1) Common
a) Cleaning substances (detergents, soap, shampoo)
b) Cough and cold remedies
c) Cosmetics
I2) Potentially lethal

a) AlcohoVAntifreeze
b) Analgesics (paracetamol, aspirin, nonsteroidal anti-inflammatory
drugs (NSAIDs), opiates)
c) Psychotropics (neuroleptics, antidepressants, hypnotics, anxiolytics,
lithium)
d) Carbon monoxide
e) Street drugs
f) Cardiovascular drugs
Key Objectives
• Perform supportive care, decontamination or prevention of further
absorption, give antidote where indicated, and enhance elimination of the
poison.
• Determine whether poisoning has occurred, the substance involved, how
severe the exposure was, how toxic it is likely to become, and the
causticity of substance.
• Discuss special considerations in the management of poisoning with
aspirin, paracetamol, tricyclic antidepressants, and methanol.
326
• Through efficient and focused data gathering:
Determine the drug or poison causing the problem, using patient's vital
signs, mental status, pupil size, appearance, smell, etc. as potential
clues in addition to history from patient, paramedics, police, clinician,
pharmacist, friends and relatives (if intentional, history is frequently
unreliable) .
• Interpret the critical clinical and laboratory findings which were crucial in
the processes of exclusion, differentiation, and diagnosis:
Select and interpret drug screen based on clinical information.
Select laboratory and diagnostic imaging investigation for toxic effects
in addition to diagnosis.
Calculate anion and osmolar gap; explain and interpret findings.
• Conduct an effective plan of management for a poisoned patient:
Perform supportive care before or at the same time as data gathering
and investigation, such as ensuring airway adequacy, haemodynamic
stability and intravenous access, cardiac monitoring and
electrocardiogram (EGG), pulse oximetry, etc.
Outline initial management in a patient with poisoning with altered
consciousness.
Discuss advantages and disadvantages of various strategies for
prevention of poison absorption (also termed decontamination) in a
patient who is less than one hour after intake of poison.
Discuss strategies for enhancing the elimination from the body of
various poisons.
327
080 Polycythaemia 1 Elevated Haemoglobin
Overview
The reason for evaluating patients with elevated haemoglobin levels (male greater
than 185 g/L, female greater than 165 g/L) is first to ascertain the presence or absence
of polycythaemia vera, and subsequently to differentiate between the various causes
of secondary erythrocytosis.
Causes
1) Polycythaemia vera -low or normal erythropoietin
2) Secondary erythrocytosis - elevated erythropoietin

a) Hypoxaemia
0 Pulmonary (sleep-apnoea, chronic obstructive pulmonary disease
(COPD), pulmonary hypertension)
0 Eisenmenger syndrome
b) Abnormal haemoglobin function
c) Erythropoietin- secreting tumour (hepatocellular, renal cell , ovarian)
d) Other (polycystic kidney, post-transplant, hydronephrosis,
androgens)
3) Relative polycythaemia (decreased plasma

volume: e.g. burns, diarrhoea)
4) Inapparent polycythaemia (increased plasma

volume: e.g. renal failure)
Key Objective
• Discuss whether the determination of red cell mass is necessary for the
diagnosis of polycythaemia or whether measurements of haemoglobin
levels convey the same information.
Determine whether the patient has any other polycythaemia-related
features.
Differentiate between causes of secondary erythrocytosis in patients
without polycythaemia-related features.
328
List indications for bone marrow biopsy.
Contrast the interpretation of low or normal erythropoietin levels to
elevated levels in a patient with polycythaemia.
Contrast arterial oxygen saturation in primary and secondary
polycythaemia.
• Conduct an effective plan of management for a patient with polycythaemia:
Select patients in need of further investigation and referral for
specialised care.
329
081 Pregnancy
081A Antepartum Care
Overview
The purpose of antepartum care is to help achieve as good a maternal and infant
outcome as possible.
Aspects for Consideration in Antepartum Care

1) Pre-conception (counsel, if possible , about pregnancy and
perform baseline investigations which may require action prior
to pregnancy - rubella immunity, full blood examination (FBE),
Papanicolaou (Pap) sme ar). Advise about folic acid ingestion
I2) Initial presentation
3) First trimester I Second trimester 1 Third trimester
4) Pre-labour (counsel for preparation of labour, and when to

present to hospital)
Key Objectives
• Determine whether the patient is pregnant and the most likely date of
conception for the purpose of estimating the date of confinement; develop
an appropriate relationship and rapport with prenatal patients.
• List physical findings associated with a normal first trimester pregnancy,
including vital signs, skin changes, breast changes, and uterine changes.
Elicit factors which might alter the expected date of conception, or
might influence the course of the pregnancy (e.g. maternal age);
determine uterine size in terms of weeks of gestation.
In the first trimester, determine whether pregnancy is progressing
satisfactorily (normal pregnancy symptoms), or complications are
present (hyperemesis, miscarriage, ectopic).
In the second trimester, determine whether pre-term labour may be
present, any bleeding, or urinary symptoms, and determine maternal
blood pressure (BP) and fetal heart rate.
In the third trimester, determine the presence of fetal movements or
their decrease, and measure BP, maternal weight gain, and determine
fetal lie and presentation.
Diagnose onset of labour.
330
Discuss current recommendations for ultrasound screening in normal
pregnancy, in second trimester, and list first trimester complications for
which ultrasound is indicated.
Discuss recommendations for routine testing at the first antenatal visit
(if not done pre-pregnancy) screening for Group B streptococcus,
diabetes, bacterial vaginosis, and maternal serum screening in
second trimester, proteinuria and glycosuria in third trimester.
List investigations for a patient with Rh-negative blood type and list
indications for anti-D globulin; list indications for amniocentesis.
• Conduct an effective plan of management for a patient who is pregnant:
Outline nutrition management in normal pregnancy including
recommendations for iron and folic acid.
List potential complications associated with smoking, alcohol in
pregnancy (maternal and neonatal).
Counsel patient on medications which are safe and unsafe during
pregnancy, physical and sexual activity, travel , vaccines and
breastfeeding.
Outline management of urinary tract infections (UTis) in pregnancy,
nausea and vomiting, and constipation.
Outline initial management of a woman with symphyseal fundal height
measurement significantly larger or smaller than expected.
Outline initial management of BP elevation, of bleeding in first, second,
or third trimester.
Outline initial management if fetal movements decline.
Outline initial management of post-date pregnancy.
Outline initial management of diabetes in pregnancy.
Counsel patients regarding breastfeeding.
Counsel patients regarding maternal serum screening.
Outline the components of the Bishop score, and the relevance of the
score in clinical practice.
Select patients in need of specialised care because of maternal or fetal
problems.
331
081 Pregnancy
081 B Intrapartum/Postpartum Care
Overview
Intrapartum and postpartum care means the care of the mother and fetus during labour
and the six-week period following birth during which the reproductive tract returns to
its normal nonpregnant state. Of pregnant women, 85% will undergo spontaneous
labour between 37 and 42 weeks of gestation. Labour is the process by which products
of conception are delivered from the uterus by progressive cervical effacement and
dilatation in the presence of regular uterine contractions.
Aspects for Consideration in Intrapartum/Postpartum Care

1) Normallabour
2) Abnormal labour
3) · Fetal surveillance
4) Postpartum care
a) Normal puerperium
b) Abnormal puerperium
0 Fever
0 Pain
0 Haemorrhage
Key Objective
• Determine whether the patient is in labour, rupture of membranes is
present, and determine her risk score.
Determine the fetal presentation, lie, position, station, and presence of
engagement.
Determine whether labour is in the latent or active phase, and state the
approximate duration of each, as well as the duration of the second
stage of labour, expected rate of cervical dilatation.
Determine whether physical findings are present which necessitate
increased levels of maternal or fetal monitoring.
List maternal and fetal signs to be monitored; discuss indications and
frequency for pelvic examination in the first and second stages of
labour.
Diagnose prolonged, protracted, or arrested stages of labour, and
factors in mother's history predisposing to them.
332
Diagnose cause of abnormal labour in terms of uterine contraction,
fetus, and passage.
Determine whether the course of the puerperium is normal or abnormal
physically and emotionally.
Differentiate between causes of postpartum fever. Include genital tract
infection, episiotomy or wound infection, urinary tract infection (UTI),
breast infection, breast engorgement, intercurrent or viral infection,
deep venous thrombosis (DVT) and/or pulmonary embolus.
Determine cause of postpartum haemorrhage (uterine, cervical,
vaginal, perineal, disseminated intra-vascular coagulation (DIC)).
Order routine tests for a woman presenting to the labour and delivery
ward.
List indications for fetal and uterine contractions monitoring and
discuss significance of meconium in amniotic fluid.
Postpartum, in an Rh-negative woman, order maternal and neonatal
blood to determine need for Rh immunoglobulin.
• Conduct an effective plan of management for a patient in labour and
postpartum:
Counsel patient in labour about need for examination, reasons for
examination, and permission to go ahead.
Describe mechanism of delivery for a fetus; define shoulder dystocia
and list risk factors for this complication.
Describe signs of placental separation and normal duration of third
stage of labour; describe the options for management of the third stage
of labour; list components of Apgar score.
Discuss techniques for pain relief in labour; list indications for and
complication of episiotomy; list the indications for and the
complications of epidural analgesia/anaesthesia.
List risk factors for Group B streptococcal disease in the neonate and
discuss use of prophylactic penicillin in labour.
List indications and contraindications of active management of third
stage of labour with intravenous (IV) or intramuscular (IM) oxytocics.
Outline initial management of primary and secondary postpartum
haemorrhage.
List methods to augment labour; list indications/complications of
Caesarean section, forceps, or vacuum extraction.
Outline management of puerperal pain, dyspareunia, bladder and
bowel dysfunction and depression.
Outline management of fever postpartum.
333
081 Pregnancy
081C Haemorrhage
(See 1t117 Vaginal Bleeding, Excessive in Amount or Irregular in Timing)
081 D Obstetrical Complications
Overview
Virtually any maternal medical or surgical condition can complicate the course of a
pregnancy and/or be affected by pregnancy. In addition , conditions arising in
pregnancy can have adverse effects on the mother and/or the fetus (e.g. babies born
prematurely account for greater than 50% of perinatal morbidity and mortality; an
estimated 5% of women will describe bleeding of some extent during pregnancy, and
in some patients, the bleeding will endanger the mother's survival).
Causes
11) Pre-existing maternal conditions
a) Hypertension
(see #0548 Pregnancy-Associated Hypertension)
b) Diabetes
c) Cardiac disease
d) Chronic renal disease
e) Thrombosis
f) Systemic lupus erythematosus (SLE)
2) Maternal conditions arising in pregnancy

a) Pregnancy-induced hypertension
(see #0548 Pregnancy-Associated Hypertension)
b) Gestational diabetes
c) Gestational thrombocytopenia
d) Thrombosis
e) Viral infections ('TORCH ' (I oxoplasmosis, Qther, Rubella,
Qytomegalovirus, Herpes simplex virus), rubella, varicella, HIV)
3) Fetal conditions arising in pregnancy

a) Large for gestational age (twins)
b) Small for gestational age
c) Structural abnormality of fetus
d) Alloimmune disease (Rh isoimmunisation)
334
4) Complications inherent to pregnancy
a) Antepartum haemorrhage
(see #11 7 Vaginal Bleeding, Excessive in Amount or Irregular in Timing)
b) Preterm labour
c) Preterm premature rupture of membranes
d) Polyhydramnios/Oligohydramnios
Key Objective
• Determine the risk factors that increase chances of complication during the
pregnancy at the initial visit for prenatal care.
Elicit history of pre-existing maternal medical conditions, history of
maternal or fetal problems in previous pregnancies, or any other
complication inherent to pregnancy.
Elicit family history, history of nutrition, alcohol, smoking, obesity, drug
use including recreational drugs, maternal age, viral infections,
previous fetal structural or immune abnormalities, bleeding, leakage of
fluid .
Perform physical examination of mother, uterine height, amount of
amniotic fluid, and other fetal parameters.
Select and order ultrasound and list ultrasound parameters of the
biophysical profile (amniotic fluid, fetal movement, fetal tone, fetal
breathing).
List indications for amniocentesis.
List investigations for specific maternal conditions including maternal
blood type and antibody screen.
• Conduct an effective plan of management for a patient with obstetrical
complications:
Outline preventive I 'improving outcome of pregnancy' programme (e.g.
smoking cessation , folic acid, betamethasone to mother when preterm
delivery imminent, screen for gestational diabetes, Rh immunoglobin to
Rh-negative women).
Outline immediate management of preterm labour and premature
rupture of membranes; diabetes.
335
082 Contraception I Pregnancy Prevention/Termination
Overview
Ideally, the prevention of an unwanted pregnancy should be directed at education of
patients, male and female , preferably before first sexual contact. Counselling patients
about which method to use, how, and when is a must for anyone involved in healthcare.
Counselling should also address prevention of sexually transmitted diseases (STDs).
Causes
1) Non-pennanent
a) Hormonal contraception (oral, injectable, morning after pill)
b) Barrier methods (diaphragm, cap, condom)
c) Intra-uterine devices
d) Other (abstinence, breastfeeding, withdrawal , rhythm method,
ovulation method)
I 2) Pennanent contraception
a) Sterilisation (male, female)
I 3) Termination
Key Objectives
• Determine whether there are any absolute or relative contraindications to
the use of hormonal contraceptives.
• If permanent contraception is being contemplated, determine the level of
determination and commitment to proceed, level of understanding of
options, and surgical or medical risks.
• If faced with an unplanned pregnancy, discuss the alternatives for
management.
Elicit obstetric and gynaecologic history and determine risk factors for
hormonal use.
Perform pelvic examination and exclude the presence of pregnancy if
appropriate.
processes of exclusion, differentiation. and diagnosis:
Order appropriate cultures, Papanicolaou (Pap) smear, and pregnancy
test if indicated.
336
Order ultrasound to determine gestational age in a pregnant woman ,
and recognise the accuracy is best the earlier the ultrasound
examination is done.
• Conduct an effective plan of management for a patient requesting
contraception, pregnancy prevention or termination:
Outline methods of contraception, risks of failure, complications, and
drug interactions.
Counsel patient about side-effects, adjustments if pill is missed, or
need to add barrier techniques.
Counsel patient on benefit of barrier contraception in conjunction with
hormonal contraception in reducing HIV transmission and STDs.
Counsel patient about failure rates of sterilisation, the importance of
family being perceived complete, and complications of various
approaches.
Counsel patient about the complications of pregnancy termination
including potential guilt/emotional concerns, the effect of subsequent
fertility and subsequent pregnancy outcome.
Present contraceptive and termination alternatives while respecting the
individual's own moral, ethical and religious beliefs.
Understand the legal position in regard to pregnancy termination, at
varying gestations, in Australia.
337
083 Prematurity
Overview
The impact of premature birth is best summarised by the fact that although less than
10% of babies are born prematurely (less than 37 weeks gestation), these births
account for greater than 50% of all perinatal morbidity and mortality. Most morbidity
and mortality is due to delivery at less than 28 weeks gestation. Overall, the outcome,
although guarded, can be rewarding given optimal circumstances and care.
Causes
Premature delivery can occur after spontaneous labour or when labour is induced
prematurely because of maternal, placental or fetal problems. In many instances the
cause of the spontaneous premature labour is unknown.
1) Fetal
a) Multiple gestation
b) Erythroblastosis and non immune hydrops
c) Congenital anomalies
I2) Placental
a) Placenta praevia
b) Placental abruption
13) Uterine
a) Incompetent cervix
b) Excessive enlargement (hydramnios)
c) Distortion (leiomyomas, septate)
14) Maternal
a) Preeclampsia
b) Premature rupture of membranes
c) Smoking, substance abuse
d) Chronic medical illnesses
e) Infections (urinary, cervical, amniotic) - Group 8 streptococcus,
herpes, 'TORCH' (Toxoplasmosis, Other, .Bubella, Qytomegalovirus,
tlerpes simplex virus), etc.
5) Iatrogenic (indicated induction of labour)
338
Key Objectives
• Contrast low birth weight (intra-uterine growth restriction} and prematurity.
• Identify risk factors for probable prematurity and initiate immediate and
appropriate care of a premature baby.
List the immediate and long term health problems faced by premature
infants.
Investigate the maternal and fetal factors which may precipitate a
premature birth.
• Conduct an effective plan of management for a premature baby:
Resuscitate and manage the health problems encountered by
premature infants.
Outline the nutritional requirements of premature infants.
Select patients in need of referral and/or specialised care for premature
infants.
Plan the care of a premature baby, born at 28 weeks of gestation, whilst
awaiting transfer to a tertiary care facility 200 km away.
Care of a baby with respiratory distress syndrome in the newborn
period.
Counsel parents about immediate and long term health problems
encountered by premature infants.
Co-ordinate healthcare facilities for the short and long term care of
premature infants.
• Conduct an effective plan of management for a patient in premature labour
at varying gestations:
Use of drugs to inhibit uterine contractions.
Use of corticosteroid and other drugs to improve pulmonary maturity.
Mode of delivery.
339
084 Prolapse I Pelvic Relaxation
(See also #1158 Urinary Incontinence, Elderly)
Overview
Patients with pelvic relaxation present in many different and often subtle ways. In
order to identify patients who would benefit from therapy, the clinician should be
familiar with the types of pelvic relaxation and the approach to the patient with symptoms
suggestive of this problem.
Causes
1) Uterine prolapse
2) Vaginal vault prolapse
3) Cystocele
'
4) Rectocele
5) Enterocele Gross procidentia
Key Objective
• Describe the progression of genital prolapse from grade one to
procidentia, including the impact of chronic straining and hormone
replacement therapy (HAT); explain to the patient the development and
progression of urinary tract or gastrointestinal symptoms.
Determine the severity of symptoms, effect on activity, predisposing
factors (particularly after the menopause), and risk factors for surgery.
Differentiate between different types of pelvic relaxation according to
associated difficulties (e.g. voiding, stress incontinence, defaecating).
Determine structure which is prolapsing on physical examination.
State that there are no specific tests for the assessment of prolapse.
• Conduct an effective plan of management for a patient with pelvic
relaxation or prolapse:
Counsel the patient on benefit and risks of no intervention,
conservative measures including pelvic floor exercises and other
physiotherapy, and surgery.
Select patients requiring referral for specialised care.
340
085 Proteinuria
Overview
Proteinuria is identified by positive dipstick on urinalysis during routine screening for
insurance and other examinations, when examining patients with symptoms related
to the urinary tract, or when following the progress of patients with secondary causes.
Persistent proteinuria implies abnormal glomerular function and always requires further
investigation.
Causes
l1) Transient proteinuria
I 2) Orthostatic proteinuria
I3) Persistent proteinuria

a) Overflow
b) Tubulointerstitial
c) Glomerular (including nephrotic syndrome)
0 Primary
• Minimal change disease
• Focal segmental glomerulosclerosis (FSGS)
• Membranous glomerulonephropathy
0 Secondary
• Diabetes mellitus
• Secondary FSGS
• Collagen diseases
Key Objective
• Differentiate between benign causes of proteinuria and proteinuria
resulting from transient or permanent glomerular damage requiring
specialist assessment.
Exclude transient and orthostatic proteinuria; reassure patients about
benign nature of conditions.
Differentiate between overflow and tubulointerstitial proteinuria, and
glomerular proteinuria.
Diagnose common primary or secondary glomerular diseases.
341
• Conduct an effective plan of management for a proteinuric patient:
State referral indications for a patient with proteinuria.
Formulate the most appropriate management to prevent or delay
progression to chronic renal failure in patients with primary glomerular
diseases.
Formulate the most appropriate management to prevent or delay
diabetic nephropathy in patients with Type I or Type II diabetes mellitus.
Interpret and contrast the prognostic significance and possible clinical
sequelae of light and heavy proteinuria.
342
086 Pruritus
Overview
Pruritus accompanies many skin disorders. In the allergic group pruritus is the
predominant symptom. In the absence of a primary skin lesion pruritus can be indicative
of systemic disease or psychological or emotional disorder.
Causes
1) Skin Lesions
a) Primary skin disease
0 Skin blisters (papular/vesicular)
• Dermatitis herpetiformis
• Bullous pemphigoid
0 Skin rash (papulosquamous)
• Mycosis fungoides
• Psoriasis
• Lichen planus
b) Parasitosis (scabies, pediculosis)
c) Allergy (atopic dermatitis/eczema, urticaria, allergic dermatitis)
d) Arthropod bites
e) Factitious dermatitis
I2) No skin lesions

a) Senile pruritus
b) Drugs/Foods
c) Obstructive biliary disease
d) Uraemia I Renal failure
e) Haematological
0 Polycythaemia vera I Microcytic anaemia
0 Leukaemia
0 Lymphoma
f) Carcinoma I Carcinoid syndrome
g) Endocrine (diabetes, thyroid disease)
3) Psychiatric, psychological and emotional disorders
343
Key Objectives
• Identify the skin disorder causing pruritus.
• In the absence of primary skin lesions identify the underlying cause of the
pruritus.
Categorise primary skin lesions associated with pruritus.
In the absence of skin lesions, select investigations to diagnose
systemic disorders.
• Conduct an effective plan of management for a patient with pruritus:
Outline local and other therapy for pruritus.
Treat underlying systemic disease if identified.
344
086 Pruritus
OB6A Pruritus Ani
Overview
Anal pruritus can be associated with defective local hygiene, generalised skin
conditions, or local anal conditions. Pruritus vulvae may coexist.
Causes
1) Defaecatory habits, poor or exeessive hygiene
2) Localised anorectal conditions (skin tags, anal condylomas/

warts, fistulae, haemorrhoids, threadworms)
3) Generalised skin or systemic disorders
Key Objective
• Conduct a detailed history and local examination to identify likely causes.
Generai/Specffic Objectives
Identify likely general causal factors (diabetes mellitus, general skin
disorders).
Perform full anorectal examination for local causes.
Detect yeasts, fungi , parasites from stool examination, skin scraping,
microscopy.
• Outline a management plan based on appropriate local hygiene.
345
087 Psychosis I Disordered Thought
Overview
Psychosis refers to a group of severe mental disorders characterised by morbid, false
beliefs (delusions), disturbances in sensory perception (hallucinations), disorganised
speech patterns (thought disorder) and grossly disorganised or catatonic behaviour.
There may be impaired or absent insight into the pathological nature of symptoms,
affective flattening, apathy and lack of drive, and cognitive and conceptual impairments.
Schizophrenia is both the most common and the classic psychotic disorder, but psychotic
symptoms in isolation can occur in a range of other syndromes. There are about
200,000 people with schizophrenia in Australia. The illness typically begins in
adolescence or early adult life and is associated with prolonged disability, stigma,
under-employment and discrimination. Depending on the severity, schizophrenia
may significantly affect the patient's social, occupational and interpersonal fu nctioning.
Causes
11) Schizophrenia (and subtypes)
2) Schizophreniform disorder (duration of illness less than six

months)
3) Schizoaffective disorders (concurrent mood disorder and

psychosis)
4) Delusional disorder (grandiose, persecutory, erotomanic,

jealous, somatic)
5) Brief psychotic disorder (duration less than four weeks)
6) Psychotic disorder due to a general medical condition
7) Substance-induced psychotic disorder - intoxication or

withdrawal from
a) Alcohol
b) Amphetamines
c) Cannabis
d) Cocaine
e) Hallucinogens
f) Inhalants
g) Opioids
h) Psychotropics
I 8) Shared psychotic d isorder
348
19) Other
IIOT niii• • IIA'laiAL

If you nNHI this you will
learn what IIIIICie me:
• So funny (say all those jokes).
• Act so cool.
• Think about girts, girls, girls so much.
• Drive with absolutely NO FEAR.
• Pay so much attention to my appearance.
• Say and do so many stupid, irrational
and dangerous things.
Etc...
Psychotic disorder
Key Objective
• Differentiate patients with psychotic symptoms who have insight and are
aware of their symptoms, from those who have no insight and are of
concern to others.
Establish a collaborative relationship with the patient.
Determine the extent of the psychotic symptoms, including the history
of onset, progression and duration and any associated mood
symptoms.
Determine any relationship between the psychotic symptoms and
medical illness, alcohol and non-prescribed drugs or medication.
Assess personality and social strengths and current level of
functioning.
Perform a mental status examination including risk of harm to self and
others.
Perform baseline screening investigations and physical examination.
Refer for appropriate educational/social/vocational assessments.
• Establish an effective plan of management for a patient with psychosis:
Outline modern management principles, including atypical
antipsychotics, psychological and psychosocial therapies and the role
of hospitalisation.
Tactfully counsel and educate patients and carers/family about the
nature and natural history of the psychosis.
Provide ongoing support to carers and family and advocacy for patients
and advise on support groups.
Select patients in need of specialised referral or rehabilitation .
347
088 Pupil Abnormalities
Overview
Pupils should be black, round, equal and reactive to light and accommodation. The
pupils dilate in dark surroundings and constrict in bright light, the size depending on a
balance between parasympathetic and sympathetic innervation. Pupil size is
influenced by local mydriatics or the effects of drugs. Any non-black area in the pupil
implies media opacification in the anterior chamber, lens or vitreous. Abnormal pupillary
reactivity and size after trauma may be important clues to intracranial pathology in the
setting of head injuries; and pupillary abnormalities may be associated with a variety
of neurological disorders.
Causes
l1) Local disorder of iris
2) Inequality of pupil size (anisocoria)

a) Impaired pupil constriction (third nerve palsy, tonic pupil, mydriatics)
b) Impaired pupil dilatation (Horner syndrome)
0 First order (hypothalamus, brain stem, spinal cord lesions)
0 Second order I Preganglionic lesions
0 Third order I Postganglionic lesions
3) Impairment of pupil constriction (without anisocoria)

a) Unilateral (optic nerve or retinal lesion)
b) Bilateral (diabetes, syphilis, midbrain lesion, hydrocephalus,
factitious)
Left Homer syndrome
348
Key Objectives
• Determine whether there has been previous ocular inflammation, trauma,
loss of vision, or eye pain in order to begin ruling out local disorders.
• Understand and interpret changes in pupillary appearance, size and
reactivity.
• Select patients in need of urgent referral.
Differentiate clinically between the various mechanisms of pupil
abnormalities.
Select patients in need of referral for further investigation.
• Conduct an effective plan of management for a patient with pupil
abnormalities:
Select patients in need of referral for management.
349
089 Regional Pain
089A Chronic Musculofascial Pain
Overview
'Fibromyalgia' (fibrositis, myofascial pain syndrome) is a very common but poorly
defined condition of unknown aetiology associated with chronic pain affecting muscles
and soft tissues such as tendons and ligaments. Symptoms include diffuse muscle
pains and aches, stiffness, fatigue, sleep disturbance and focal points of tenderness
without other abnormalities on physical examination, laboratory, or radiological studies.
Concomitant anxiety and depression are common. The condition is more common in
women.
Polymyalgia rheumatica is a rheumatic condition that is frequently linked to giant cell
(temporal) arteritis. Polymyalgia rheumatica is a relatively common disorder, with a
prevalence of about 700 out of 100,000 persons over 50 years of age. Synovitis is
considered to be the cause of the discomfort. The erythrocyte sedimentation rate
(ESR) is markedly raised in most patients.
Causes
j1) 'Fibromyalgia'
j 2) Polymyalgia rheumatica
I 3) Polymyositis/Dermatomyositis
Flat foot
350
4) Shoulder pain (rotator cuff injury, capsulitis, bursitis, tendinitis)
5) Hand/Wrist pain (carpal tunnel, fracture/dislocation, tendinitis)
6) Foot pain (flat feet, hallux valgus, metatarsalgia, neuroma,

fasciitis, stress fracture, tendinitis, apophysitis)
7) Knee pain (meniscal injury, cruciate/collateralligament injury,

patellofemoral disease)
I 8) Nerve entrapments I Neuropathies
Key Objectives
• Differentiate between articular and non-articular pain.
• Differentiate between 'fibromyalgia' and polymyalgia rheumatica.
Diagnose 'fibromyalgia', especially in women, from history and
associated features, especially tender point examination of selected
anatomic locations.
Diagnose polymyalgia rheumatica in patients 50 years or older with
bilateral morning stiffness and aching (more than 30 minutes) for at
least one month in neck or torso, shoulders or proximal arms and hips
or proximal thighs, and an elevated ESR.
Differentiate local from referred pain, acute from chronic, muscle from
nerve pain, etc.
• Interpret critical cli nical and laboratory findings which were key in the
State that laboratory tests in patients with 'fibromyalgia' are normal,
and in polymyalgia rheumatica only the sedimentation rate is usually
elevated.
List indications for electromyelography (EMG).
• Conduct an effective plan of management for a patient with regional pain:
Outline management of 'fibromyalgia' including exercise, education,
medication, and supportive psychosocial measures.
Describe complications of corticosteroids and nonsteroid anti-
inflammatory agents.
List indication and contraindications in management of non-articular
conditions of: rest, physiotherapy, anti-inflammatory medication, local
corticosteroid injection, and surgery.
351
089 Regional Pain
0898 Low Back Pain
Overview
Low back pain is an extremely common complaint. Most people experience at least
one episode of acute low back strain at some period. Short-lived back pain of
mechanical origin is not associated with a clearly definable aetiology. Most low back
pain is of benign aetiology, with spontaneous recovery over the course of days or
weeks. Imaging and other investigations are unnecessary and unlikely to be helpful.
Concerning features, indicating the need for further investigation, include an insidious
onset, a neurologic deficit, unremitting severe pain, evidence of systemic illness and
a relevant medical history. Associated loss of bladder or bowel control indicates a
potential surgical emergency. Low back pain remains a major cause of lost work time.
In many patients with persisting and chronic back pain a precise pathological diagnosis
is not possible. Chronic occupationally-related and litigation-linked low back pain
may be associated with unconscious or conscious exaggeration of symptoms in the
absence of demonstrative organic disease and with the presence of non-objective
physical signs indicating abnormal illness behaviour.
Causes
1) Acute musculoligamentous lumbo-sacral strain - self resolving
2) Chronic, persistent or recurrent low back pain

a) Mechanical
Age-related and degenerative spondylosis
• Disc disease and prolapse, osteoarthritis of facet joints
• Spondylolysis, spondylolisthesis, spinal canal stenosis
U Metabolic (osteoporosis)
0 Neoplasms (myeloma, metastasis)
0 Spinal infections (tuberculosis (TB), osteomyelitis)
0 Inflammatory (seronegative spondyloarthropathy)
• Ankylosing spondylitis
• Reiter syndrome I Reactive arthritis
• Enteropathic arthrit!s
• Psoriatic arthritis
b) Referred pain (renal, pancreatic, vascular aneurysm, retroperitoneal
blood, gynaecologic, etc.)
Key Objectives
• Perform an appropriately focused and accurate examination of back and
spine.
• Recognise the rare serious causes of low back pain by being alert to
warning flags in history and examination.
352
Determine whether inciting event exists, pain location, radiation , and
effect of back or leg motion.
Perform examination of the back and proximate anatomic areas that
could lead to back pain.
Identify patients with neurologic defect.
Determine whether there is loss of sphincter tone or urinary retention ,
and state that the presence of such signs represent a surgical
emergency.
Outline management of acute back pain without neurologic or other
abnormality on examination.
Outline clinical features and management plans in a patient with low
back pain with nerve root impingement.
353
089 Regional Pain
089C Neck Pain
Overview
Attacks of transient acute neck pain and stiffness are very common, the incidence
increasing with age. Prolonged neck pain and stiffness are important sequelae to
whiplash-associated motor vehicle collisions. Specific nerve root deficiencies are
rarely found. Continuing chronic disabilities and impairments are often associated
with compensation claims and secondary psychological problems.
Causes
1) Intrinsic disease
a) Muscle spasm (awkward posture, certain occupations- assemblyline
workers, violinists)
b) Disc degeneration/herniation (with neural impingement, C6-C7 most
commonly)
c) Osteoarthritis I Cervical spondylosis
d) Tumours
e) Other (whiplash, myofascial pain syndromes, diffuse idiopathic
skeletal hyperostosis, congenital spinal stenosis)
2) Systemic disease (rheumatoid arthritis (RA), ankylosing

spondylitis, polymyalgia rheumatica, bone metastases)
3) Referred (from shoulder, angina pectoris, meningitis,

diaphragm, or teeth and jaw pathology)
Key Objectives
• Determine whether the pain is caused by conditions that are intrinsic to the
cervical spine or its musculature, by systemic conditions or by referred
pain from elsewhere.
Elicit a history including age, occupation, trauma, radiation of pain (if
not correlated with neuro-anatomic pathways, consider myofascial pain
or 'fibromyalgia').
Determine whether pain is nerve root, and which root, or whether the
condition is central disc herniation with bilateral long tract signs.
Determine muscle and sensory function, tendon reflexes, neck mobility,
trigger points.
354
State that imaging (computed tomography (CT), magnetic resonance
imaging (MAl)) may demonstrate significant lesions in asymptomatic
patients.
Select diagnostic imaging when indicated.
List indications for electromyelography (EMG).
• Conduct an effective plan of management for a patient with cervical pain:
Outline conservative medical management for degenerative disc
disease (posture modification, cervical collar, physical therapy, local
pain relief, drugs, trigger point injections, etc.).
388
089 Regional Pain
0890 Facial Pain
Overview
Facial pain can be separate from or can overlap with headache. Pain in the face itself
has a miscellany of causes from local disorders. Referred pain from intracranial,
cardiac and other causes needs to be excluded; the keys to accurate diagnosis are a
careful history and physical examination aimed at recognising urgent causes and
those requiring additional investigation.
Causes
1) Dental pain (caries, third molar impaction, root abscess, etc.)
2) Sinuses (maxillary, frontal and ethmoid sinusitis)
I 3} Eye problems (glaucoma, iritis)
4) Temporomandibular joint (TMJ) dysfunction
5) Nasopharyngeal and oesophageal causes (inflammations, foreign

body, neoplasms)
6) Migraine variants (facial migraine, cluster headaches)
7) Salivary gland disorders (sialitis, stone, neoplasm)
8) Trigeminal neuralgia ('tic douloureux')
9) Referred pain from extrafacial (intracranial, cardiac) causes
Key Objectives
• Differentiate causes by careful history-taking
and examination.
• Recognise referred pain from extrafacial
causes.
Parotitis
356
089 Regional Pain
089E Shoulder Pain
(See also #071A Pain in the Upper Extremities)
Overview
Shoulder pain is commonly associated with painful limitation of arm movement, which
aids identification of pain due to intrinsic shoulder disease from that referred from
neck, diaphragm and mediastinum. Osteoarthritis of the glenohumeral joint is
uncommon and in most instances the pain is due to rotator cuff problems, bursitis and
acromioclavicular arthritis. The mobility of the joints associated with shoulder
movements renders them liable to dislocation and recu rrent dislocation, especially
from sporting injuries.
Causes
1) Rotator cuff lesions I Subacromial bursitis
2) Adhesive capsulitis ('frozen shoulder' )
I 3) Bicipital tendinitis/tear
I 4) Acromioclavicular arthritis
I 5) Referred pain
a) lschaemic cardiac disease I Pericarditis
b) Cervical spondylosis
c) Gallbladder I Diaphragm
d) Pancoast tumour
Key Objectives
• Diagnose most likely cause from history and examination.
• Exclude extrinsic causes of shoulder pain.
• Recognise requirements for investigation and specialised care.
357
089 Regional Pain
089F Hand/Wrist/Elbow Pain
Overview
Pain in the upper limb involving hand, wrist or elbow is a common symptom, usually
definable by careful history and examination into well-defined causes, and responding
well to treatment. A smaller subgroup of pred_ominantly functional illness linked with
repetitive strain, of poorly defined aetiology and often associated with work-related
compensation claims, is more difficult to treat.
Causes
1) Nerve entrapment/impingement syndromes
a) Carpal tunnel (median nerve at wrist)
b) Ulnar neuritis (cubitus valgus, Guyon canal, ' ulnar hammer'
syndrome)
c) Cervical spondylosis I Disc prolapse with nerve root radiculopathy
d) Thoracic outlet syndrome with nerve root radiculopathy
I2) Stenosing tenosynovitis

a) de Quervain tenosynovitis
b) Trigger finger
Trigger finger
I 3) Musculotendinous strain injuries

a) Lateral and medical epicondylitis ('tennis elbow', 'golfer elbow')
358
14) Degenerative
a) Rheumatoid arthritis (RA) (wrist/hands/fingers)
b) Osteoarthritis (hands/thumb/fingers)
Z-thumb deformity
5) Vascular
a) Raynaud syndrome, scleroderma
b) Venous thrombosis (axillary vein thrombosis I effort thrombosis)
c) Arterial thromboembolism (cervical rib, thoracic outlet syndrome,
distal vascular effects)
d) Lymphoedema
Calcinosis - scleroderma
16) Referred pain (cardiac, lung apex)
7) Reflex sympathetic dystrophy (chronic regional

pain syndrome, Sudeck atrophy)
Key Objectives
359
089 Regional Pain
089G Hip Pain

(See also #059 Joint Pain, Mono-Articular (Acute, Chronic) and
#061 Limp 1 Pain in Lower Extremity in Children)
Overview
Causes of pain in the hip tend to be age related . In childhood , a variety of potentially
severe disorders can benefit from early diagnosis and treatment. In adults osteoarthritis
is the most common cause of hip pain. Pain in the region of the hip can also be
referred from the lumbar spine and sacro-iliac joints. lschaemic claudicant muscle
pain secondary to aorto-iliac occlusion can be confused with joint pain.
Causes in Children
1) Developmental dysplasia of hip (DDH, CDH)
2) Juvenile osteochondritis of femoral head (Legg-Calve-Perthes

disease)
I 3) Septic arthritis
4) Transient synovitis ('irritable hip')
I 5) Slipped femoral head epiphysis
Causes in Adults
11) Osteoarthritis of hip
2) Osteonecrosis of femoral head (steroids, decompression

sickness, previous dislocation)
3) Musculofascial strain/bursitis ('snapping hip', trochante ric

bursitis)
4) Ref erred pain from othe r extra-articular causes

a) Lumbar disc prolapse
b) Cutaneous nerve entrapment (meralgia paraesthetica)
c) lschaemic aorto-iliac vascular disease
360
Osteoarthritis of hlp
Avascular necrosis femoral heads
Key Objectives
361
089 Regional Pain
089H Knee Pain
Overview
The knee is the most complex and extensive of all body joints, and is the area of most
active bone growth in childhood. The knee and adjacent long bones are the most
common sites for osteomyelitis and primary bone tumours in ch ildhood. The knee is
particularly vu lnerable to injuries in contact sports such as football ; and depends for its
stability on strong ligaments and the surrounding muscles, particularly quadriceps
femoris. Surrounding bursae are prone to inflammatory complications. Osteoarthritis
presents with painful stiffness, the incidence increasing with advancing age.
Causes
1) Osteoarthritis I Rheumatoid arthritis (RA)
J 2) Traumatic derangements
a) Meniscal, and crucial/collateral ligamentous damage
b) Traumatic chondromalacia of patella or condyle
c) Traumatic osteochondritis dissecans I osteonecrosis
d) Traumatic musculoligamentous strains (extensor apparatus injuries,
Osgood-Schlatter apophysitis)
3) Bursitis (prepatellar, pretibial, anserine, semimembranosus,

Baker cyst)
4) Vascular disease - popliteal aneurysm
I 5) Referred pain (hip)
Key Objectives
• Recognise requirements for investigation and specialised care (including
arthroscopy).
362
089 Regional Pain
0891 Foot and Ankle Pain
Overview
Apart from ischaemic pain and proximal neuropathies, which are important to exclude,
most causes of chronic foot pain are due to local abnormalities. Chronic foot strain is
exacerbated by obesity and improper footware.
Footcare in diabetics to prevent ulce rative neuropathic, ischaemic, and infective
complications has a high priority in preventive primary care practice.
Causes
1) Forefoot pain (metatarsalgia)
a) Anterior flat foot, hallux valgus, bursitis ('bunion ')
b) Claw toe I Hammer toe I Over-riding toe
c) Plantar digital neuritis/neuroma ('Morton metatarsalgia')
d) Stress fracture ('march fracture'), metatarsal necks
e) Plantar warts/callosities
f) lschaemic and neuropathic pain (diabetes, atheroma)
I 2) Heel and ankle pain

a) Plantar fasciitis
b) Achilles tendinitis/bursitis/tear
c) Peroneal tendinitis/dislocation
d) Tarsal tunnel syndrome
e) Traumatic osteochondritis/osteonecrosis
0 Calcaneum (Sever)
0 Navicular (Kohler)
0 Metatarsal (Freiberg)
Key Objectives
• Diagnose most likely causes from history and examination.
• Recognise cases needing investigation and specialised care.
363
089 Regional Pain
089J Spinal Compression I Osteoporosis
Overview
Spinal compression is one manifestation of osteoporosis, the prevalence of which
increases with age. As the proportion of our population in old-age rises, osteoporosis
becomes an important cause of painful fractures, deformity, loss of mobility and
independence, and even death.
Causes
1) Type I (oestrogen/testoste rone deficiency or menopause-
=
ratio male:female one:six)
2) Type II (age related- ratio male:female =one:two)

13) Disuse
a) Lack of weight-bearing activity (inactivity, prolonged bed rest)
b) Paralysis I Paresis I Weightlessness in space
14) Diet
a) Malnutrition I Anorexia nervosa (inadequate calcium I vitamin C,D I
protein)
b) Alcoholism I Smoking
I 5) Chronic disease
a) Rheumatoid arthritis (RA)
b) Drugs (increased cortisol, heparin, methotrexate)
c) Genetic (peak bone mass, osteogenesis imperfecta)
d) Metabolic acidosis
e) Neoplasms (myeloma/lymphoma)
I 6) Endoc r ine causes

a) Hyperparathyroidism (HPT) I Hyperthyroidism
b) Hypercortisolism
364
Key Objectives
• Define osteoporosis as a metabolic bone disease with decreased density
(mass/unit volume; bone is abnormally porous and thin). The reduced
bone mass weakens the mechanical strength of the bone, thus making it
much more likely to break, often with little or no trauma.
• Outline how osteoporosis and its complications can be prevented or
minimised.
In a patient with spinal compression or other fractures, determine
extent of trauma causing break or whether the fracture occurred at rest
or routine activity.
Determine the presence of spinal deformity (kyphosis), loss of height,
and abdominal protrusion.
Differentiate osteoporosis from osteomalacia (defective bone
mineralisation)
Check for risk factors of osteoporosis.
• Interpret critical clinical and laboratory findings that were key in the
Select patients requiring investigation for less common causes of bone
loss.
Select patients in need of bone density assessment to prevent or
minimise osteoporosis.
• Conduct an effective plan of management for a patient with osteoporosis
and/or spinal fracture:
Outline management of pain relief in vertebral compression fractures
as well as supportive measures and mobilisation.
Outline prevention and treatment of osteoporosis including nutrition,
calcium and vitamin D supplementation, drug (oestrogen,
biphosphonates) therapy, and activity.
365
089 Regional Pain
089K Cancer Pain
(See also #030 Dying Patient)
Overview
The most common cancers causing death in Australia are lung, bowel, breast, prostate,
lymphoma and pancreas. Chronic pain is a major symptom in many or most patients
with advanced cancer. Doctors dealing with such patients must appreciate the principles
of global palliative care combined with adequate pain control and prevention. Broad-
spectrum analgesic management using an 'analgesic ladder' approach to maximise
analgesic effect is required.
Use of adjuvant analgesics, psychotropic medications, laxatives when using opioid
analgesics, and anti-emetics form part of this approach. All cancer patients requiring
analgesics need close and compassionate supervision to achieve maximum comfort
with minimal adverse effects.
Causes
Pain can be associated with most cancers; the most common associations in Australia
are with lung, bowel, breast, prostate, lymphoma and pancreas.
366
Agents used for pain relief in cancer patients
1) Non-opioids (paracetamol, nonsteroidal anti-inflammatory
drugs (NSAIDs))
12) Weak opioids (codeine, etc.)
13) Strong opioids (morphine)
4) Adjuvant (non-conventional) analgesics

a) Steroids
b) Antidepressants
c) Anticonvulsants
d) Muscle relaxants
e) Nerve transmission blockade (transcutaneous electrical nerve
stimulation (TENS), acupuncture, epidural injection, implantable
devices)
Key Objective
• Maintenance of maximum pain control with the lowest attainable adverse
effects.
367
090 Renal Failure, Acute (Anuria/Oliguria I Acute Renal
Failure (ARF))
Overview
A sudden and rapid rise in serum creatinine is a common finding. A competent clinician
is required to have an organised approach to this problem. Prompt diagnosis and
treatment of extrarenal causes can prevent progression to established acute renal
failure (ARF).
Causes
1) Pre-renal causes of oliguria/azotaemia
a) Hypovolaemia (haemorrhage, volume loss, third space loss)
b) Distributional shock (sepsis)
c) Cardiac causes of hypotension (myocardial infarction (MI))
d) Obstructive causes of hypotension (pulmonary embolus)
2) Renal causes of oliguria/azotaemia

a) Glomerular (crescentic glomerulonephritis, haemolytic uraemic
syndrome (HUS), etc.)
b) Tubular (acute tubular necrosis (ATN))
c) Tubulo-interstitial
_J Acute interstitial nephritis (drugs, toxins)
_J Cast nephropathy
d) Vascular (e.g. malignant hypertension, renovascular disease)
3) Post-renal causes of oliguria/azotaemia

(prostate obstruction, cervical cancer, stone, etc.)
14) Drugs
Key Objectives
• Contrast the clinical findings of acute and of chronic renal failure, and
determine whether the serum creatinine rise is primarily acute or chronic,
or an acute problem superimposed on a chronic one.
• Identify treatable extrarenal causes and correct these.
368
After determining that the rise in serum creatinine is caused by an
acute problem (or acute superimposed on chronic), differentiate pre-
renal, from renal , and post-renal ARF.
Select appropriate laboratory and diagnostic imaging investigations.
Compare results, and discuss which of the three types of ARF is most
likely.
• Conduct an effective plan of management for a patient with ARF:
In patients suspected of having post-renal failure, select the insertion of
a patent urethral catheter as an initial investigative as well as
therapeutic measure; institute early ultrasound of upper urinary tract if
anuria/oliguria confirmed.
Outline initial management of fluid and dietary restrictions in a patient
with ARF.
Select initial intervention(s) in the management of complications of
ARF.
Outline indications for renal and peritoneal dialysis.
Outline principles of haemodialysis and haemofiltration.
389
091 Renal Failure, Chronic
Overview
Although specialists in nephrology will care for patients with chronic renal failure,
generalist clinicians will care for other common medical problems that afflict these
patients. Clinicians must realise that patients with chronic renal failure have unique
risks and that common therapies may be harmful because kidneys are frequently the
main routes for excretion of many drugs.
Causes
1) Pre-renal causes
a) Renal vascular disease (occlusion)
b) Cholesterol emboli
I 2) Renal causes
. a) Glomerular diseases, primary (focal segmental glomerulosclerosis
(FSGS), immunoglobulin A (lgA) nephropathy)
b) Glomerular diseases, secondary (diabetic nephropathy, hypertensive
nephropathy, systemic lupus erythematosus (SLE))
c) Chronic interstitial nephritis
d) Polycystic kidney disease
3) Post-renal causes (obstructive nephropathy)
370
Key Objective
• Determine which patients with elevated serum creatinine levels have
chronic rather than acute renal failure (ARF), and communicate as early as
possible to such patients that progression to chronic renal failure may be
avoided or delayed with conservative management. Select such patients
for referral.
Diagnose chronic renal failure, its underlying aetiology, and associated
complications.
• Conduct an effective plan of management for a patient with chronic renal
failure:
Outline secondary prevention management for chronic renal failure.
List indications and contraindications for dialysis in chronic renal
failure.
Counsel and educate patients about secondary and tertiary prevention
strategies.
Counsel and educate patients about choosing to start chronic
dialysis I preparation for renal transplantation.
Outline principles of management for patients with irreversible renal
failure.
371
092 Rhinorrhoea I Sore Throat
Overview
Rhinorrhoea and sore throat occurring together indicate a viral upper respiratory tract
infection (URTI) such as the 'common cold', transmitted by infected saliva or nasal
secretions. Sore throat alone may be caused by bacterial pathogens particularly
Group A streptococci, when specific therapy is indicated. Rhinorrhoea alone is not
infective and may be seasonal (hay fever or allergic rhinitis) or chronic (vasomotor
rhinitis).
Causes
1) Infections (viral, bacterial, mycoplasma, Chlamydia, candidiasis)
2) Noninfectious chronic rhinitis and allergic rhinitis
3) Obstruction (foreign body in nasal passage, polyps, deviated

septum)
I 4) Neoplasm
Key Objectives
• Discuss that making a clinical diagnosis of streptococcal tonsillo-
pharyngitis is difficult, but excluding the diagnosis is easier in the presence
of rhinorrhoea, cough, hoarseness, and normal temperature. Such
patients usually have a viral URTI and do not require diagnostic tests or
treatment.
• Discuss the benefit of antibiotic treatment in Group A streptococcal
pharyngitis with respect to prevention of acute rheumatic fever and acute
glomerulonephritis.
Determine whether testing for Group A streptococci is indicated.
Determine if an allergy or more unusual cause for rhinorrhoea is
present.
Select th roat culture of the posterior pharynx in patients suspected of
having streptococcal infection, or rapid antigen detection test.
372
• Conduct an effective plan of management for a patient with rhinorrhoea
and/or sore throat:
Outline the management of contacts of patients with proven
streptococcal infections.
Outline management in a patient with streptococcal, non-streptococcal
URTI or other causes for symptoms.
373
093 Scrotal Mass
Overview
A swelling confined to the scrotum must be differentiated from an inguinoscrotal swelling
in continuity (virtually diagnostic of an indirect inguinal hernia). Most true scrotal
swellings are benign, often requiring only reassurance. Tumours of the testis are
uncommon (only one to two percent of malignant tumours in men), but represent a
very important tumour in young men (20-40 years). Advances in management have
markedly improved survival rates.
Causes
1) lnguinoscrotal swelling (indirect inguinal hernia)
I 2) True scrotal swelling

a) Cystic (transilluminable)
0 Hydrocele (primary, secondary)
0 Epididymal cyst (spermatocele)
b) Venous (soft, compressible)
0 Varicocele (almost invariably left-sided, lessens on recumbency)
c) Solid (firm, non-transilluminable)
0 Testicular malignancy
• Seminoma
• Teratoma
• Mixed
• Lymphoma
• Other
0 Epididymitis
0 Chronic bacterial (tuberculosis (TB))
0 Granulomatous orchitis I Testicular
abscess
Varicocele
374
Key Objectives
• Differentiate true scrotal swellings from inguinoscrotal swellings (check for
reducibility of inguinoscrotal indirect inguinal hernia).
• Differentiate benign scrotal masses from those suspicious of testicular
tumour.
• Differentiate solid true scrotal swelling (testicular tumour until disproved)
from :
Benign cystic swelling (trans-illuminates):
* Hydrocele - surrounds testis.
.. Epididymal cyst - above and behind testis .
Varicocele (soft squishy 'bag of worms' feel, lessens on recumbency) .
• Differentiate secondary hydrocele hiding tumour, from primary hydrocele
(younger age, use of ultrasound and tumour markers as diagnostic aids) in
suspicious presentations.
• Distinguish between suspicious and non-suspicious lumps.
Non-suspicious - primary hydroceles in older patients, epididymal
cysts also mainly in older patients.
Suspicious - all solid masses of testis and epididymis.
• Differentiate from primarily painful lesions (see #094 Scrotal Pain (Acute)).
• Recognise importance of avoiding scrotal needling/aspiration of
suspicious lumps.
• Selection of suspicious lumps needing scrotal ultrasound; abdominal,
pelvic and chest computed tomography (CT) scanning; and search for
tumour markers.
• Elicit history of undescended testicle, infertility, previous testicular tumour,
breast enlargement/tenderness.
Perform abdominal examination including inguinal areas, and an
examination of the male genitalia (erect and supine), including rectal
examination to assess the prostate and seminal vesicles in suspicious
lumps.
Select patients for CT scanning of chest, abdomen, and pelvis.
• Conduct an effective plan of management for a patient with a scrotal mass:
Outline management options for masses which are not testicular
tumours.
375
094 Scrotal Pain (Acute)
Overview
Most scrotal swellings are painless. Acutely painful swellings mandate early diagnosis
and treatment. Occasionally pain precedes or is independent of a scrotal mass.
Torsion-prone testis with horizontal lie
Causes
11) Torsion
a) Torsion of testis
b) Torsion of testicular appendage
12) Inflammation
a) Acute epididymitis, orchitis, trauma
13) Tumours
a) Acute haemorrhage into testicular tumour
4) Conditions arising outside scrotum

a) Acute strangulation of inguinoscrotal hernia
b) Referred pain - renal 'col ic'
376
Key Objective
• Acute scrotal pain accompanied by a tender testis is a surgical emergency
caused by testicular torsion. The diagnosis is either confirmed or excluded
by urgent operation ('Look and see' rather than 'Wait and see').
Distinguish testicular torsion from acute epididymitis by:
* Operative findings (operation mandatory if any doubt exists).
* Rapidity of onset (minutes versus hours).
* Age group (children or young adults versus older patients).
* Absence of urinary symptoms.
* Ultrasound, nuclear scan (occasionally helpful with equivocal
presentations, must not delay urgent surgery).
Elicit history of dysuria, sexual contacts; examine genitalia, prostate
and abdomen.
Distinguish true scrotal masses from inguinoscrotal masses.
Define indications and contraindications for nuclear medicine blood
flow or Doppler ultrasound studies.
• Develop an algorithm outlining a plan of management for a patient with
scrotal pain:
Outline natural history of testicular torsion and predisposing factors,
and time limits of ischaemia tolerated before infarction.
Outline management of epididymitis.
377
095 Seizures (Epilepsy)
Overview
Seizures are an important differential diagnosis of syncope. A seizure is a transient
neurological dysfunction, with symptoms and signs resulting from excessive, abnormal
electrical discharge of cortical neurons. Clinical manifestations include disturbances
of consciousness, emotion, sensations, motor functions and behaviour. Epilepsy is a
chronic condition characterised by recurrent seizures, comprising a heterogeneous
group of disorders with multiple causes and manifestations. Most patients with epilepsy
have more than one type of seizure. A precise diagnosis of epilepsy requi res the
integration of all clinical data including seizure type; electroencephalographic and
imaging findings; age of onset; aetiology; family history; precipitating factors and
pathophysiology.
The International League Against Epilepsy Classification

1) Partial (focal, local) seizures
a) Simple partial seizures (consciousness not impaired)
0 With motor symptoms
0 With somatosensory or special sensory symptoms
0 With autonomic symptoms
0 With psychic symptoms
b) Complex, partial seizures (with impaired consciousness)
0 Beginning as simple partial, with or without automatisms, and
progressing to impairment of consciousness
0 With no other features
0 With features as in simple partial seizures
0 With automatisms
c) With impairment of consciousness at onset
0 With no other features
0 With features as in simple partial seizures
0 With automatisms
d) Partial seizures evolving to secondarily generalised seizures
0 Simple partial seizures evolving to generalised seizures
0 Complex partial seizures evolving to generalised seizures
0 Simple complex seizures evolving to complex partial seizu res to
generalised seizures
2) Generalised seizures (convulsive or nonconvulsive)

a) Absence seizures; either typical or atypical
b) Myoclonic seizures
c) Clonic seizures
d) Tonic seizures
378
e) Tonic-clonic seizures
f) Atonic seizures
3) Unclassified epileptic seizures including neonatal seizures,

rhythmic eye movements, chewing and swimming movements
Causes of Seizures
11) Partial seizures (focal seizures)
2) Partial seizures complex (temporal lobe or psychomotor)
3) Generalised tonic-clonic (grand mal) seizure

a) Idiopathic (20%)
b) Trauma
c) Infectious
d) Vascular I Hypertension (malignant, eclampsia)
e) Neoplasia
f) Degenerative
g) Metabolic
0 Electrolyte abnormalities
0 Alcohol or drug .withdrawal
0 Renal or liver failure
I 4) Absence (petit mal) seizure
I 5) Pseudoseizures
I 6) Status epilepticus
Key Objective
• Differentiate syncope from disturbances of cerebral function caused by a
seizure.
379
Differentiate between a true seizure and pseudoseizure.
Differentiate between partial seizures and generalised seizures.
Determine which seizures may be secondary to co-existing medical
problems.
Contrast findings in patients with focal seizures, complex partial
seizures, generalised seizures, and petit mal seizures.
Compare findings in syncope with cerebral seizures.
• Conduct an effective plan of management for a patient with seizures:
Formulate a plan of management for a patient with status epilepticus.
Contrast the plan of management of petit mal seizures with grand mal
and partial seizures.
Select patients in need of specialised care and/or referral to other
Outline educational and/or supportive counselling for patients with
seizure disorders including concerns for psychosocial impact,
considerations for employment, and driving.
380
096 Sexual Maturation
096A Sexual Maturation, Normal
Overview
The normal process of sexual maturation, with some acceptable variations, requires
the integration of normal central neNous system (CNS) (hypothalamus, pituitary),
gonadal, and adrenal fu nction along with a critical body mass and nutrition level.
Clinicians familiar with the normal process are in a better position to discern abnormal
sexual maturation.
Causes
Processes required for normal growth and maturation in males and females:
Normal sexual maturation results primarily from the integration between the various
components of the endocrine system and the gonads.
Key Objective
• Differentiate acceptable variations which occur in male and female
progress to puberty and sexual maturation, from abnormal sexual
maturation.
Elicit pertinent data regarding birth, infantile growth, and development
and its impact upon puberty.
Assess the normal sequencing of pubertal development through
Tanner stages 1 to 5 for both males and females.
Outline the use of growth charts and Tanner staging in the assessment
of children.
Outline initial evaluation of variations from the expected patterns of
sexual maturation.
• Conduct an effective plan of management for a patient with normal or
accepted variations of sexual maturation:
Counsel adolescents and their parents about the normal progression
to sexual maturation.
381
096 Sexual Maturation
0968 Sexual Maturation, Abnormal
(See also #063A Amenorrhoea (also Oligomenorrhoea))
Overview
Sexual development is important to adolescent perception of self-image and well-
being. Many factors may disrupt the normal progression to sexual maturation.
Causes
1) Delayed puberty (failure of Stage II: male by 14 years, female
by 13 years; or menarche within five years of breast budding)
a) Growth failure I Delayed puberty overlap
0 Multiple endocrine disorders
0 Variants of normal/constitutional
0 Systemic diseases
b) Central causes
0 Congenital (hypothalamic/pituitary - low
gonadotropins or low gonadotropin-
releasing hormone (GnRH))
• Syndromes (Prader-Willi,
Laurence-Moon-Biedl)
• Malformations (midline development
defects)
• Isolated deficiency of gonadotropins I
panhypopituitarism
0 Acquired
• Infection I Trauma I Tumours
(craniopharyngioma, pituitary
adenoma)
• Malnutrition I Chronic systemic
disease
c) Primary gonadal disorders
0 Congenital
• Chromosomal (Turner syndrome,
Klinefelter syndrome)
• Gonadal differentiation I Biosynthetic
defects
0 Acquired
• Infection (oophoritis, orchitis)
• Trauma, torsion Delayed puberty
382
• Neoplasms I Neoplasia therapy (irradiation, cytotoxic drugs) I
Surgery
d) Interruption I Lack of completion
0 Testicular feminisation
0 Mullerian duct abnormalities (absenUhypoplastic uterus/vagina)
2) Precocious puberty (female before 8 years; male before 10 years)

a) Central
0 Constitutional (gonadotropin dependent I gonadotropin independent)
0 Central nervous system (CNS) (neoplasms, post-inflammatory,
neurofibromatosis, hydrocephalus)
0 Hypothyroidism, McCune-Albright syndrome
3) Pseudoprecocious puberty (incomplete)
14) Other
Key Objective
• Counsel patients and their families about the need for immediate or
delayed screening, referral or careful followup.
Differentiate between the principal causes of abnormal sexual
development.
Identify features of delayed and precocious puberty; differentiate
delayed puberty versus growth failure.
Evaluate patients with suspected abnormal sexual development with a
minimum of investigations.
• Conduct an effective plan of management for a patient with abnormal
sexual maturation:
Outline initial management and counsel both caregivers and patients
with abnormal sexual development.
097 Sexual Concerns and Gender Identity Disorder
Overview
The social appropriateness of sexuality is culturally determined. The clinician's own
sexual attitude needs to be recognised and taken into account in order for the clinician
to deal with the patient's concern in a relevant manner. The patient must be set at ease
in order to make possible discussion of private and sensitive sexual issues.
Causes
1) Sexual dysfunction in the male or female
a) Premature ejaculation I Ejaculatory failure
b) Erectile dysfunction (impotence)
c) Anorgasmia
d) Dyspareunia
e) Inhibition of sexual desire
f) Vaginismus
2) Sexual paraphilias (exhibitionism, fetishism, voyeurism,

transvestism, sadomasochism, paedophilia)
I 3) Lesbian and gay patients
I 4) Disabled patients and sexuality
5) Children/Adolescents; sexuality and gender identity
I 6) Ageing patients and sexuality
j 7) Gender identity in adults
Key Objectives
• Elicit factors precipitating and maintaining the sexual concern , effort to
escape the concern, and relevant medical history to rule out reversible
organic conditions.
• Determine the patient's social and physical sexual development and
behaviour as well as the patient's sexual orientation and comfort with it.
384
Differentiate mutual or normal sexuality from dysfunctional sexuality,
sexual abuse or assault, and incest.
Determine whether there is correlation between experiential desire
and physiological response.
Perform focused examination including neurologic examination with
emphasis on peripheral neuropathy and examination of genitalia.
Select patients requiring hormone assays.
• Conduct an effective plan of management for a patient who has sexual
concerns:
Pseudohennaphroditism
385
098 Shock I Hypotension
Overview
Shock is an acute and potentially life-threatening clinical emergency with multiple
causes leading to broadly similar clinical syndromes associated with failure of vital
organ and tissue perfusion. All clinicians must be fami liar with principles of recognition,
diagnosis and treatment of shock as a life-threatening emergency with plans
appropriate to rapid clinical identification and treatment of the most common causes;
and selective use of clinical and laboratory investigations to identify those cases
refractory to initial management. Hypotension , although common to many types of
shock, is one aspect only of the clinical syndrome.
Causes
1) Cardiogenic
a) Myocardial infarction (MI)
b) Cardiomyopathy
I 2) Hypovolaemic
a) Haemorrhage- overt or concealed blood loss
b) Plasma loss- burns, peritonitis
c) Water and electrolyte loss
0 Gastrointestinal losses
0 Interstitial (third space) losses
0 Skin losses (burns, hyperthermia)
I 3) Obstructive
a) Pulmonary embolism
b) Tension pneumothorax
c) Pericardia I tamponade, constrictive pericarditis
d) Aortic dissection, venacaval obstruction
j 4) Distributive
a) Septic
b) Anaphylaxis
c) Vasovagalsyncope
d) Spinal injury I Autonomic blockade I Drugs
e) Endocrine- pituitary, adrenal, thyroid deficiencies
386
Key Objectives
• Recognition of key features of shock (pallor, hypotension, thready pulse,
oliguria) as a life-threatening acute clinical emergency.
• Ability to formulate rapidly diagnostic and management plans and
strategies appropriate to the various causative agencies in a practical and
logical sequence.
• Through rapid, efficient, focused data gathering:
Recognise and diagnose shock states.
Formulate integrated diagnostic and management plans to differentiate
and deal with the various causes.
• Identify critical clinical and investigational findings which are key in the
process of diagnosis, exclusion, differentiation, and monitoring of
response to treatment.
• Use the above to formulate a flow chart covering the effective diagnosis,
management and monitoring of a patient with shock.
• Outline the principles and specifics of the management plans of a patient
with:
Hypovolaemic shock.
Cardiogenic shock.
Septic shock.
'Refractory' shock.
• Identify patients with shock requiring use of central venous pressure or
pulmonary wedged capillary pressure monitoring.
387
098 Shock I Hypotension
09BA Anaphylaxis
Overview
Anaphylaxis causes a significant number of fatalities per year, and occurs in 1 in 5,000
hospital admissions. Children most commonly are allergic to foods.
Causes
1) Drugs
a) Beta-lactam antibiotics
b) Nonsteroidal anti-inflammatory drugs (NSAIDs)
c) Anti-neoplastic medications
d) Angiotensin-converting enzyme (ACE) inhibitors
2) Hymenoptera (bees, wasps) envenomation
3) Radiographic contrast media
4) Blood products
5) Foods (seafood, milk, nuts)
6) Latex
Key Objectives
• Differentiate anaphylaxis from conditions which are similar such as shock
from other causes , other flush syndromes, 'restaurant syndrome',
increased endogenous histamine production, acute respiratory failure
syndromes, or non-organic syndromes such as panic attacks or
Munchausen stridor.
• Initiate therapy by ensuring airway, intubation if necessary, establishing
intravenous lines with large bore needles, stop antigen administration, and
select pharmacologic agents.
388
Perform examination for skin involvement (90% have pruritus, urticaria,
angio-oedema, flushing) , upper and lower respiratory tract involvement
(50%), shock or conduction disturbances (30%), gastrointestinal or
nervous system involvement.
• Conduct an effective plan of management for a patient with anaphylaxis:
Outline initial management for anaphylaxis.
Outline rationale for use of epinephrine, glucagon, antihistamines,
steroids, and beta-agonists in aerosols for respiratory symptoms.
Discuss biphasic anaphylaxis and protracted anaphylaxis.
389
099 Sudden Infant Death Syndrome (SIDS)
(Acute Life-Threatening Event (ALTE))
Overview
Sudden infant death syndrome (SIDS) and/or acute life-threatening event (ALTE) are
devastating events for caregivers and healthcare workers alike. It is imperative that
the precursors, probable cause and parental concerns are extensively evaluated to
prevent recurrence.
Causes
l11 Idiopathic
I 2) Prolonged apnoea
I 3) Response to hypoxia/hypercarbia
I 4) Upper airway obstruction
I 5) Abnormal sleep patterns
I 6) Cardiac arrhythmias
I 7) Face-down position
Key Objectives
• Evaluate fully the possible causes of an infant history of ALTE or SIDS.
• Counsel the parents and families of such children.
• Provide management of children who are at risk for ALTE or SIDS.
Determine whether there is evidence of possible risk factors or causes
known to be associated with ALTE or SIDS.
Diagnose the infant presenting with ALTE or SIDS.
390
Evaluate fully, but with compassion and empathy, the possible causes
of the infant presenting with ALTE or SIDS.
• Conduct an effective plan of management for a patient with ALTE or SIDS:
Perform immediate resuscitative measures.
Conduct short/long term bereavement management for parents/family.
Select patients in need of referral and/or consultation for infants and
families at risk, i.e. bereavement issues, genetic counselling.
Select patients who are in need of child protection (if appropriate).
39 1
100 Skin and Subcutaneous Lesions
100A Focal Skin Lesions - Benign Lesions
Overview
The majority of focal skin lesions are manifestly benign longstanding lesions of
congenital or acquired origin requiring no treatment. An important group of benign
lesions are dysplastic and premalignant.
Focal skin lesions can usually be rapidly assessed on clinical grounds into:
• Clearly benign skin lesions.
• 'Suspicious' lesions.
Causes of Clearly Benign Focal Skin Lesions
In Children (macules, nodules or papules):

1) Pigmented lesions
a) Vascular malformation
ll 'Port wine stain' (capillary haemangioma)
(J 'Strawberry naevus'
(cavernous haemangioma)
b) Benign melanocytic naevi ('common moles')
0 Junctional
u Intradermal
u Compound
c) Common freckle (ephelis)
d) Uncommon lesions
0 'Blue naevus' (Mongolian spot)
0 Juvenile melanoma
I2) Other Lesions

a) Viral infective wart- verruca vulgaris
b) Pyogenic granuloma
Blue naevus
392
In Adults (macules, nodules or papules):
1) Pigmented lesions
a) Benign melanocytic naevus
0 Junctional
0 Intradermal
0 Compound
b) Seborrhoeic keratosis (seborrhoeic wart)
c) Campbell de Morgan spot (senile haemangioma, cherry angioma)
d) Dermatofibroma (sclerosing haemangioma, histiocytoma)
e) Spider naevus
f) Senile freckle (lentigo)- macular
g) Senile purpura - macular
Benign melanocytic naevus
Spider naevus Seborrhoeic keratoses
393
12) Non-pigmented lesions
a) Skin tag {soft fibroma, benign squamous papilloma)
b) Solar keratosis {hyperkeratosis, senile keratosis - premalignant)
c) Callosity {callus)
d) Xanthoma
e) Vi ral infective wart - verruca vulgaris
Solar hyperkeratoses
Key Objective
• Identify clearly benign skin lesions on the basis of their clinical features
and distinguish between the various types.
Identify clearly benign lesions not requiring treatment and provide
appropriate reassurance.
Identify premalignant lesions.
Discuss risk factors, prevention and treatment of premalignant lesions.
Identify lesions requiring treatment and outline management plans.
394
1008 Focal Skin Lesions- 1Suspicious' Lesions
Overview
Malignant and premalignant skin lesions are common in Austral ia with a susceptible
population and excessive solar exposure. Malignant melanoma is virtually unknown
in children but occurs throughout adult life; its frequency in Australia and in most other
countries is increasing. Basal and squamous cell cancers occur in older patients and
multiple lesions are common. Preventive measures against excessive solar exposure
(e.g. 'Slip, Slop, Slap' UV-protection campaign) comprise important public health
measures.
Causes of 'Suspicious' Focal Skin Lesions

1) Basal cell carcinoma (BCC)
Various morphologic types
a) Nodular
b) Ulcerative
c) Cystic
d) Psoriatic
e) Comedoform
f) Sclerosing/Cicatrising
g) Pigmented
NodularBCC
Clcatrlsing sec
Ulcerative sec
395
I 2) Squamous cell carcinoma (SCC)
a) SCC-in-situ (Bowen disease)
b) Invasive SCC
Bowen disease
Ulcerative SCC
3) Keratoacanthoma (molluscum sebaceum)
Keratoacanthoma
I 4) Malignant melanoma
a) Hutchinson melanotic freckle (lentigo maligna)
b) Superficial spreading melanoma
c) Nodular melanoma
d) Amelanotic melanoma
396
Hutchinson melanotic freckle
Superficial spreading melanoma
Nodular melanoma
I 5) Other suspicious lesions

a) lnfected/Traumatised benign lesions
b) Pyogenic granuloma
c) Kaposi sarcoma (haemangiosarcoma)
d) Lymphoma of skin (mycosis fungoides)
e) Dermatofibrosarcoma protuberans
f) Cancer - metastatic skin deposits, acanthosis nigricans
(paraneoplastic skin reaction)
g) Merkel cell tumour (rare malignancy from sensory dermal cells)
397
Pyogenic granuloma
Mycosis fungo/des of trunk Kaposi sarcoma
Key Objectives
• Identify suspicious skin lesions and refer appropriately for diagnostic
excision.
• Differentiate between different types on basis of history and examination.
• Discuss natural history and spread of common skin malignancies.
• Discuss management plans by surgery and adjuvant means.
• Discuss indications for and technique of biopsy of suspicious skin lesions.
• Discuss indications for surgical excision of skin lesions (cosmetic, irritative,
prophylactic, suspicion of malignancy).
• Discuss pathology of malignant melanoma.
• Discuss types of benign and malignant pigmented lesions and indications
for excision.
398
100C Focal Subcutaneous Lumps
Overview
A subcutaneous lump is a very common cli nical problem. Most are of longstanding;
the vast majority are benign lesions. Distinction on clinical grounds alone can almost
always be made between the four most common lesions: lipomas, cysts, ganglia and
bursae.
Causes
11) Lipomas
Very common. Present as benign slow-growing, soft,
painless lobulated subcutaneous swellings
occurring anywhere there is fat.
Variants
a) Unusual sites- sub-fascial,
intramuscular (IM), breast, bowel
(submucosal)
b) Multiple painless subcutaneous
lipomas of limbs or trunk
(sometimes familial)
c) Retroperitoneal liposarcoma - locally
invasive and malignant
12) Cysts
a) Keratinous ('sebaceous' or
'epidermoid') cysts
Very common. Derived from pilosebaceous follicle
- found anywhere there is hair: particularly scalp,
scrotum. Rounded, smooth contour and skin
attachments (not always with a punctum) distinguish
cysts from lipomas.
Variants and complications:
0 Infection - Cock peculiar tumour
0 Accretion - 'seborrhoeic' horn
0 Desiccation and plaque formation -
pilomatrixoma (Malherbe calcifying
epithelioma)
b) Implantation 'dermoid' cyst- traumatic
'Sebaceous' cyst
0 Overlying puncture wound or scar
c) Inclusion 'dermoid' cyst- developmental
0 In ventral midline head and neck, and at lateral angles of eyes
399
13) Ganglia
Common deeper subcutaneous swellings around joints or tendon sheaths of the
wrists, fingers and ankles.
Variants:
a) Synovial (mucous) cyst of fingers on dorsum of terminal phalanx
b) Compound palmar and dorsal ganglia of w rist tendon sheaths
Mucous cyst of finger Ganglion of foot
14) Bursae
Sited around tendon insertions or over bony
prominences (olecranon, prepatellar,
pretibial, ischial, anserine) and may
communicate with joints (suprapatellar,
subacromial). May develop as adventitious
de novo swellings at any site of abnormal
friction (bunion).
Olecranon bursitis
Key Objective
• Differentiate between most common lesions (lipomas, cysts, ganglia and
bursae) from history, physical findings and anatomical localisation.
Compare and contrast physical characteristics of lipomas and
keratinous cysts.
List common bursae presenting with clinical problems.
Define which subcutaneous lumps will require diagnostic investigation
to clarify diagnosis.
Define which subcutaneous lumps will require surgical excision.
400
1000 Red, Hot, Tender, Swollen Skin and Subcutaneous

Layers
Overview
Red , hot, tender, swollen skin and subcutaneous tissues suggesting cellul itis and
other spreading infections of skin and subcutaneous layers comprise important and
common clinical presentations in primary care and in hospital emergency departments
and wards. Causative organisms are commonly staphylococcal or streptococcal via a
skin breach. Oedematous limbs are at increased risk.
Injured and ischaemic tissues predispose to serious necrotising anaerobic infections
of skin and deeper tissues , from a wider range of infecting organisms. These infections
are more common after devitalising injuries , in diabetic patients and immune-
compromised hosts, and as postoperative complications after abdominal and vascular
operations. Severe life-threatening infections such as necrotising fasciitis and clostridial
myositis ('gas gangrene') require early radical excisional debridement and drainage
as well as antibiotics.
Causes
1) Cellulitis and erysipelas
Web space infection in diabetic foot
401
2) Necrotising infections of skin and subcutaneous tissues
a) Fournier gangrene (spreading necrotising panniculitis)
b) Necrotising fasciitis
c) Clostridial myonecrosis ('gas gangrene')
d) Other (Meleney ulcer I synergistio gangrene, pyoderma
gangrenosum, anthrax)
Fournier gangrene perineum and scrotum
Necrotising anaerobic fasciitls back
Pyoderma gangrenosum
402
Key Objectives
• Early recognition of cellulitis/erysipelas and differentiation from other
erythematous skin conditions.
• Early recognition of serious necrotising infections.
Identify signs of cellulitis/erysipelas and check for predisposing factors
(skin wound/abrasion, chronic venous or lymphatic oedema, arterial
insufficiency, underlying osteomyelitis), signs of local spread
(ascending lymphangitis, lymphadenopathy) and general effects (fever,
tachycardia) (see also #0348 Unilateral Limb Oedema (Swollen
Limb)).
Recognise signs of severe necrotising anaerobic infection (impending
skin necrosis, subcutaneous crepitus, generalised toxicity).
Discuss methods of identifying causative organisms.
Discuss role of imaging in diagnosis.
• Outline management plans for the effective treatment of infections of skin
and subcutaneous tissues.
Recognise the vital role of excisional surgery and drainage in
management of necrotising infection.
Discuss choice of antibiotic and routes of administration.
Discuss role of adjuvant hyperbaric oxygen treatment
403
101 Skin Blisters - Boils - Comedones - Ulcers
Overview
Comedones are a feature of the very common skin disorder of acne vulgaris. Acne
affects many teenagers and is associated with chronic inflammation of blocked
pilosebaceous follicles and seborrhoea. Boils (furuncles) are acute staphylococcal
abscesses developing in hair follicles. Carbuncles form more extensive sub-cutaneous
abscesses, often with inadequate drainage. Both boils and carbuncles are commoner
in diabetic patients. Blistering or vesiculobullous disorders include a wide range of
conditions and can be considered according to their incidence. The less common
causes may require histology and immunofluorescence studies.
Causes
1) Comedones, papules and pustules
a) Acne vulgaris -very common
b) Furuncle/Carbuncle
c) Impetigo
d) Scabies, insect bites, etc.
Acne vulgaris Scabies
2) Vesicles I Vesiculobullous disorders - common

a) Herpes simplex
b) Varicella
c) Herpes zoster
d) Contact dermatitis
0 Plants
0 Industrial agents
Other chemicals
404
Herpes zoster Ophthalmic
herpes zoster
e) Insect bites
f) Dyshidrotic eczema (pompholyx)
g) Burns
3) Vesicles I Vesiculobullous disorders - uncommon

a) Drug eruptions
b) Bullous pemphigoid
c) Bullous erythema multiforme
d) Dermatitis cutanea tarda
4) Vesicles I Vesiculobullous disorders - rare

a) Epidermolysis bullosa
b) Pemphigus
c) Linear immunoglobulin A (lgA) disease
d) Cicatricial pemphigoid
e) Toxic epidermal necrolysis
f) Bullae of diabetes, renal failure
Epidermolysis bul/osa
405
Key Objective
• Recognise and differentiate common and important skin disorders
presenting as comedones, papules, pustules, blisters and vesicles.
Determine areas of involvement, type of patient, and associated
findings.
Differentiate between types of lesion.
Select patients in need of further investigation.
• Conduct an effective plan of management for a patient with skin blisters:
Outline management for common and important skin conditions.
• Conduct an effective plan of management for a patient with a furuncle or
carbuncle.
• Conduct an effective plan of management for a patient with acne vulgaris.
406
101 Skin Blisters - Boils - Comedones - Ulcers
101A Chronic Leg Ulcer
Overview
Chronic leg ulcers can be due to many causes; but the three most common causes
are: chronic deep venous insufficiency ('venous ulcer'), arterial ischaemia ('arterial
ulcer') and diabetes mellitus ('diabetic ulcer'). The site and appearance of the ulcer
will often establish the diagnosis. A host of less common causes exists. Aims in
treatment are initially to heal the ulcer and subsequently to prevent recurrence.
Causes
1) 'Venous ulcer'- chronic deep venous insufficiency
(post-thrombotic syndrome)
Chronic venous ulcer
2) 'Arterial ulcer'- arterial ischaemia

(macrovascular/microvascular)
lschaemic ulcer
407
3) 'Diabetic ulcer' - usually of primarily neuropathic origin;
ischaemia and infection will often also contribute
I4) Less common causes

a) Infective ulcer
0 'Tropical ulcer'
0 Mycobacterium ulcerans
('Bairnsdale ulcer')
Pyogenic and synergistic
infections
b) Vasculitis complicating systemic
and immunodeficiency states
0 Rheumatoid arthritis (RA) ,
polyarteritis neurosa
0 Inflammatory bowel disease (lBO)
0 Haemoglobinopathies
Severe hypertension ('Martorell
ulcer')
0 Microembolisation from proximal
arterial/valvular lesions
c) Malignant ulcer- squamous cell
carcinoma (SCC)
0 Complicating chronic burn scar Tropical ulcer
('Marjolin ulcer'), chronic venous
ulceration or osteomyelitis
CJ Kaposi sarcoma (often AIDS-related)
0 Melanoma
d) Other neuropathic ulcers
U Alcoholism , peripheral neuropathy, leprosy, syringomyelia, spina
bifid a
e) Insect bites (e.g. wolf spider)
f) Healing failure of traumatic ulcers
Skin flap avulsions in elderly
0 Sites of intravenous drug use
g) Self-inflicted (factitious) ulceration
408
Key Objectives
• Appreciate and recognise the characteristic features from each of the most
common causes; venous disease, arterial disease and diabetes.
• Formulate diagnostic and management plans related to individual causes.
Recognise symptoms and signs of chronic venous insufficiency
associated with chronic venous ulceration with ambulatory superficial
venous hypertension: fibrotic induration, oedema, pigmentation and
venous eczema, and ankle flares.
Recognise local features of ischaemic arterial ulcers.
Perform appropriate assessment of arterial supply of limb by
examination of circulation and capillary refilling , aided by clinical tests
(Buerger, ankle/arm systolic index).
Assess for relative contributions of neuropathy, infection,
macrovascular and microvascular disease in patients with diabetes.
Be alert to other potential causes of chronic leg ulceration and
formulate diagnostic, investigational and management plans for
patients with leg ulcers due to various causes.
Consider self-inflicted (factitious) ulceration in ulcers with atypical
appearance, site or response to treatment.
409
102 Skin Rash
-- - - - -
1 Dermatitis
- -- - - -
102A Skin Rash I Dermatitis and/or Fever, Urticaria 1

Angio-Oedema
Overview
Skin rashes are often identified by thei r location and distribution as well as their
morphology.
Causes
l1) Dry/Scaly rash
a) Atopic dermatitis
b) Nummular dermatitis
c) Pityriasis rosea
d) Psoriasis
e) Seborrhoeic dermatitis
f) Microsporum canis infection ('ringworm')
Atopic dermatitis 'Ringworm' of face
410
I 2) Moist/Macerated rash
a) Candidiasis
b) Tinea cruris
c) Tinea pedis
d) Tinea capitis
e) Contact dermatitis
I
3) Urticaria I Angio-oedema
a) Acute urticaria (greater than two-third of cases, self-limited,
recurrence lasts less than six weeks)
b) Chronic urticaria (one-third of cases, recurrence lasts greater than
six weeks)
0 Associated with triggers (aetiology not identified in up to 90% of
patients)
• Drugs (antibiotics, hormones, nonsteroidal anti-inflammatory
drugs (NSAIDs), aspirin, local anaesthetics, opiates, angiotensin-
converting enzyme (ACE) inhibitors)
• Physical contact (animal saliva, plant resins, latex, metals, lotions,
soap)
• Insect stings- risk of anaphylaxis (bees, wasps, hornets)
• Latex - risk of anaphylaxis if sensitised (gloves, condoms,
balloons)
• Aeroallergens (oral allergy syndrome)
• Foods and additives (only 10% if placebo controlled)
• Infections (greater than 80% of urticaria in paediatric patients)
Drug eruption - smoxyc/1/ln
411
0 Associated with angie-oedema (50% of urticaria, both acute and
chronic)
0 Associated with systemic disease
• Systemic lupus erythematosus (SLE)
• Henoch-Sch6nlein purpura
• Cryoglobulinaemia
• Autoimmune thyroid disease
• Mastocytosis
• Urticarial vasculitis
Facial rash - SLE
Key Objectives
• Categorise skin problems by rash type, configuration and the distribution
of the lesion.
• Determine whether the condition is acute, chronic or a manifestation of a
systemic illness based on lesion resolution, length of occurrence, and
clinical picture.
Elicit a detailed history and physical examination including timi ng of
symptom onset, duration of lesions, identification of precipitants.
• Interpret critical clinical and laboratory findings wh ich were key in the
Select patients in need of further investigation and specialised care.
• Conduct an effective plan of management for a patient with a skin rash:
Outline management for common skin conditions.
• Select patients in need of specialised care.
412
102 Skin Rash 1 Dermatitis
1028 Childhood Communicable Diseases with or without

Skin Rash
Overview
Communicable diseases are common in childhood and vary from mild inconveniences
to life-threatening disorders. Clinicians need to differentiate between these common
conditions and initiate management specific to the cause.
Causes
1) Presenting with a rash
a) Viral (measles, rubella, roseola, varicella, herpes zoster, herpes
simplex, molluscum contagiosum ('water warts'))
b) Bacterial (meningococcal septicaemia, scarlet fever, 'scalded skin '
syndrome, impetigo, staphylococcal or streptococcal toxic shock
syndrome)
c) Other (mycoplasma infection)
Molluscum contaglosum
2) Presenting with sore throat I

a) Viral (infectious mononucleosis)
b) Bacterial (diphtheria, streptococcal)
3) Presenting with diarrhoea
413
Key Objectives
• Recognise early those life-threatening presentations involving a skin rash.
• Describe the principles of immunisation procedures.
• Determine the incubation period and possible route of communication of
the underlying disease.
• Outline measures of prevention to contain the spread of communicable
disease.
Identify the presenting features of the rash , sore throat or diarrhoea;
and identify and treat possible cases of meningococcal septicaemia
and other life-threatening conditions.
Determine the immunisation status of the infants/children.
Determine history of contacts, travel, farm visits, ingestion of
unpasteurised milk or uncooked meat, source of water supply.
When dealing with an infant, consider prenatal issues, especially
maternal history of infection.
Evaluate fully the individual and contacts of individuals with sexually
transmitted diseases (STDs).
Describe rapid viral testing, stool tests, and viral serology.
• Conduct an effective initial plan of management for a patient with a
childhood communicable disease:
Outline the procedure for immunisation and for immunising an
incompletely immunised child.
Outline management of specific communicable diseases.
414
103 Speech and Language Abnormalities I Dysphonia I
Hoarseness
Overview
Speech disorders present in all age groups, central causes being more common in
the elderly whi le non-neurological articulation disorders present more frequently in
younger patients.
Causes
1) Receptive disorders (hearing/deafness)
I 2) Central disorders
a) Aphasia- speech apparatus intact
(see #050 Hemiplegia I Hemisensory Loss I Stroke with or without
Aphasia I Prevention of Stroke)
b) Mental retardation
I 3) Articulation disorder
a) Nasal I Badly articulated I Slurred speech
0 Soft palate with or without other muscles paralysis (myasthenia,
multiple sclerosis)
0 Bulbar/Pseudobulbar palsy (amyotrophic lateral sclerosis)
0 Tongue paralysis I Macroglossia (cranial polyradiculitis, allergic
oedema)
b) Disorders of speech rhythm/timing/audibility (Parkinson disease,
multiple sclerosis, cerebellar lesions, dementia, etc.)
Laryngeal carcinoma
415
c) Speech apparatus lesions
0 Hoarseness
• Inflammation (infection, allergy, abuse/misuse, smoking, alcohol)
• Neoplasms (laryngeal benign/malignant)
• Recurrent nerve (thyroidectomy/parathyroidectomy, tumour)
0 Stammer/Stutter
0 Open nasal speech (soft palate paralysis, cleft palate)
0 Dysphasic (in deafness)
d) Silent/Non-speaking (catatonia, depression, brainstem encephalitis,
functional)
Key Objectives
• Determine whether the speech apparatus is intact and the speech disorder
is centrally determined.
• Determine whether neurological deficits are present.
Elicit information indicative of inflammation/infection, voice abuse or
misuse, smoking or alcohol.
Determine whether there is dysphagia, cough , haemoptysis, or
dyspnoea.
Conduct physical examination of head and neck.
Select patients to receive routine investigations or in need for
laryngoscopy referral.
• Conduct an effective plan of management for a patient with speech and
language abnormalities:
Outline management plan for common causes of speech disorders
(e.g. voice rest, fluids and humidity, anti-reflux therapy, no smoking).
416
104 Spinal Injuries
Overview
The most common spinal fractures are wedge crush fractures of vertebral bodies
(osteoporosis, malignancies). Spinal cord injuries from trauma result from motor vehicle
accidents (MVA), falls , sports-related trauma , or assault with weapons. The average
age at the time of spinal injury is approximately 35 years , and men are four times more
likely to be injured than are women. The sequelae of such events have a major impact
on society in terms of the cost of rehabilitation and long term care, litigation and
liability. Initial immobilisation and maintenance of ventilation are of critical importance.
Causes
1) Traumatic or pathological fractures/dislocations
of the vertebral column
I 2) Penetrating injury
I 3) Acute disc rupture
4) Ruptured arteriovenous malformation
I 5) Spontaneous epidural haematoma
Vertebral crush fracture
417
Key Objectives
• Understand how to triage and manage patients with potential or actual
acute spinal injury and make an appropriate examination of such patients.
• Provide an appropriate plan of management for the patient with acute
spinal cord compression or transection.
• Contrast the impairment of ventilatory muscle strength in the case of
complete or incomplete cervical spinal cord injury, and explain the effect of
denervation of abdominal musculature.
• State that respiratory impairment and susceptibility to respiratory
complications are greater with more cephalad injuries of the spinal cord.
Determine whether there is any impediment of respiratory function .
Elicit history about mechanism of injury and examine structures in the
spine which have been damaged.
Perform examination of spine, motor power in arms and legs,
sensation, superficial and deep tendon reflexes .
Select diagnostic imaging for assessment of spinal stability.
Outline diagnostic imaging of the lungs in patients with spinal cord
injury (e.g. upright films are often contraindicated).
• Conduct an effective plan of management for a patient with spinal injuries:
Conduct education of people at risk for prevention of spinal injuries
(diving into shallow water, skiing out of control , injuries associated with
rugby and Australian League football , cross-checking from
behind in hockey, drinking and driving, etc.).
List indications for immobilisation; for bladder catheterisation.
Initiate and maintain 'spinal precautions' and 'log rolling' of patients;
outline methods available for stabilising the spine.
List indications for steroid treatment; list analgesic drugs to use.
Counsel and support patient and family including access to
rehabilitation programmes.
418
105 Splenomegaly
Overview
A normal spleen is not palpable, so that a palpable spleen is virtually always indicative
of an underlying problem unless it is confused with the left lobe of the liver or an
enlarged left kidney.
Causes
1) Congestive- (liver cirrhosis, portal thrombosis)
I 2) Infective
a) Viral- hepatitis, glandular fever (Epstein-Barr virus (EBV)),
cytomegalovirus (CMV)
b) Bacterial - bacterial endocarditis, brucellosis, septicaemia
c) Protozoal- malaria, leishmaniasis
d) Fungal- histoplasmosis
3) Neoplastic (chronic leukaemia, lymphoma, myeloproliferative

disorders, myelofibrosis)
4) Associated with haemolysis (acquired and congenital

haemolytic anaemia)
5) Inflammatory (Still disease, Felty syndrome)
6) I nfiltrations - sarcoid, amyloid, lipid storage disorders
Key Objectives
• Perform an abdominal examination for splenomegaly and differentiate an
enlarged spleen from the left kidney or left lobe of the liver.
• In a patient with splenomegaly, determine whether it is associated with
hepatomegaly.
Determine whether stigmata of chronic liver disease, an infective
process (e.g. fever, chills, lymphadenopathy, Osler nodes, etc.), weight
loss, anaemia or jaundice are present in order to differentiate between
causes of splenomegaly.
419
processes of exclusion, differentiation, and diagnosis; and important in
Select and interpret laboratory investigations for various causes of
splenomegaly.
• Conduct an effective plan of management for a patient with splenomegaly:
Recognise that management depends on the underlying cause.
420
106 Strabismus and/ or Amblyopia
Overview
'Cross-eye', 'squint' or 'wandering eye' conditions are usually obvious and will often
lead to early medical advice being sought. However, poor vision in one eye is often
not noted until a much later stage when the possibility of significant visual impairment
is high. Both types of presentations require specialist advice.
Causes
1) Esotropia (convergent, internal, cross-eye)- congenital and
acquired
2) Exotropia (divergent, external, wall-eye)- congenital and

acquired
3) Vertical strabismus
4) Mechanical restriction
5) Convergence insufficiency
6) Amblyopia without strabismus
Key Objectives
• Determine the type of strabismus and the necessary timing of intervention.
• Screening of infants for poor vision as early as possible when suspected.
Identify relevant fam ily history.
Differentiate pseudostrabismus (lid configuration or negative angle
kappa or markedly positive angle kappa) from true strabismus.
Conduct an examination of visual acuity, ocular movement, and failure
of alignment by the cover/uncover test.
Manage and reassure where appropriate.
• Select patients with true strabismus and/or amblyopia for specialised care.
42 1
107 Substance Abuse/ Addiction
107A Substance Abuse I Drug Addiction/Withdrawal
Overview
Alcohol and nicotine abuse are such common conditions that virtually every clinician
is confronted with their complications.
Causes
11) Alcohol
I 2) Nicotine
3) Benzodiazepines, sedative-hypnotic, anxiolytic
4) Opioids
5) Cannabis
6) Cocaine
7) Hallucinogens
8) Inhalants
9) Amphetamines
10) Performance drugs
Key Objective
• Determine whether the patient is in need of emergency care because of
withdrawal symptoms or other complications.
Determine past and recent quantity and frequency of abuse, severity of
abuse and dependence, readiness to change or denial, complications
of use, family history, past treatment history, support network, and
withdrawal symptoms; identify social problems such as assault and
impaired driving.
Define limits of non-hazardous alcohol; differentiate social from
problem drinking/dependence.
Examine for mental function , weight loss, route of administration,
neurologic examination, signs of use.
422
Select patients for toxicology screening, liver function if suspected of
alcohol abuse and contrast sensitivity and specificity with 'CAGE'
questions:
* Have you felt the need to Cut down on your drinking?
* Have you felt ~nnoyed by criticism of drinking?
* Have you felt Guilty about your drinking?
* Do you feel the need for an Eye opener in the morning?
• Conduct an effective plan of management for a patient with substance
abuse:
Outline spectrum of treatment options including mutual/self-help, low-
intensity outpatient treatment, non-medical detoxification and
residential treatment, medically supervised detoxification and intensive
inpatient treatment.
Outline office counselling for mild to moderate alcohol dependence
(reviewing assessment findings, set drinking goals, conduct of periodic
followup) .
Outline alcohol withdrawal management, indications and
contraindications for disulfiram, and naltrexone, methadone; outline
management of withdrawal from opioids and benzodiazepines.
Outline management for stopping nicotine including advice to quit,
nicotine replacement therapy, setting quitting dates, behavioural
counselling, information about community resources.
Discuss guidelines for safe prescription writing for benzodiazepines
and opioids.
Outline management of cardiovascular complications of cocaine and
alcohol.
Outline prevention, detection and management of infectious
complications of intravenous (IV) drug use including hepatitis B, C, and
HIV.
4%3
107 Substance Abuse/Addiction
1078 Pathological/Problem Gambling
Overview
Gambling is the act of staking money or some other item of value on the outcome of an
event determined by chance. It is an accepted leisure pursuit enjoyed by the majority
of adult Australians. Problem gambling may affect one to three percent of the adult
population. Two-thirds of problem gamblers are men, who typically present in their
thirties (women present later) and have problems with continuous forms of gambling
such as poker machines (slots), off-course agency betting, casino or internet gaming
or the stock market.
Problem gamblers are preoccupied with gambling and have needed to use increasing
amounts of money or goods to continue. They have had repeated unsuccessful
attempts to cut back, control or stop their gambling. They tend to gamble more when
they are losing to chase their losses and then rely on others to provide the money to
relieve the desperate financial situations created by their gambling. They gamble to
escape personal or work problems or to relieve dysphoria, anxiety or depression.
They frequently lie to conceal the extent of their gambling involvement, and many will
have jeopardised or lost a significant relationship or career opportunity as a result.
Many will have committed illegal acts such as forgery, fraud, theft or embezzlement to
finance their gambling, and 20% will make a serious attempt at suicide. Bipolar
patients may gamble excessively when in a manic phase. Problem gambling has a
strong association with alcohol abuse and antisocial personality.
Key Objective
• Determine whether the pattern of gambling behaviour has disrupted the
individual's personal, family or vocational pursuits and impaired social and
occupational functioning.
Through efficient and focused data gathering:
• Elicit history and pattern of gambling behaviour from onset to the present.
• Clarity reasons for current presentation.
• Establish impact of gambling on spouse, family, work and social
relationships .
• Identify individual triggers for problem gambling behaviour.
• Elicit associated illegal behaviours to maintain gambling behaviour.
• Recognise and treat comorbid psychiatric disorders, especially mood
disorders, substance abuse, attention deficit hyperactivity disorder and
personality disorders.
• Refer for appropriate financial and psychological counselling.
• Provide ongoing psychological support to the family.
424
108 Suicidal Behaviour/Prevention
Overview
Suicidality is a spectrum ranging from suicidal ideation to self-harm to completed
suicide. Suicide is a conscious fatal self-destructive act, which although grievous, is
relatively rare. Suicidal ideation and intent may fluctuate unpredictably over brief
periods of time. Suicidal behaviour has no single cause but a conjunction of many
biopsychosocial and cognitive factors. Hypofunction of brain serotonin systems may
explain some suicidal behaviour.
About 2,000 Australians commit suicide each year and at least 20,000 deliberately
harm themselves annually. Most people who commit suicide have visited a doctor
(either clinician or psychiatrist) in the weeks prior to the act. Knowledge of the major
risk and protective factors for self-harm, as well as the predisposing and precipitating
events, is essential for appropriate early identification and management in primary
care. Survivors, including health professionals, are left traumatised and with a confused
spectrum of emotions.
Major Causal Risk Factors

1) Previous deliberate self-harm
a) Organised plan
b) Access to means
I 2) Psychiatric disorder
a) Major depression
b) Bipolar disorder
c) Other disorders including dysthymia
d) Substance abuse
e) Schizophrenia I Schizoaffective disorder especially command
hallucinations
f) Personality disorder
g) Panic/Anxiety disorder
h) Organic mental disorders (delirium, anorexia nervosa)
I 3) Socio-cultural factors
These include:
Living alone; older age; male; unmarried/separated marital status; family
history of suicide; physical illness -terminal disease, chronic pain, HIV-AIDS,
chronic neurological disorders; rural versus urban - access to support
networks; unemployed/unskilled; indigenous aboriginal Australians; recent
or anniversary loss life event; environmental influences.
425
4) Cognitions of hopelessness and helplessness
5) Previous history of violence and/or impulsivity
6) Recent disposal of assets and preparation of a legal will

.
Key Objective
• Determine whether suidde or a self-harm attempt is likely by assessing
risk factors for suicide and patient's mental state. Suicide prediction has a
low degree of sensitivity and specificity.
• Through sensitive and comprehensive data gathering, which may include
interviewing other informants:
Elicit history of risk factors, suicidal ideation and intent, content,
duration, frequency, plan and rehearsal.
Determine current stress factors and recent life events.
Determine whether a support network is available and accessible.
Recognise that risk of self-harm is increased if the patient is depressed,
psychotic or intoxicated and has established a plan with the means
available.
• Conduct an effective plan of management for a patient with suicidal
ideation:
'
Outline immediate management of a patient at imminent risk for self-
harm (e.g. local crisis psychiatric services, urgent or involuntary
hospitalisation, specialist assessment). Patient safety is paramount
and continuous observation is essential whilst arrangements are put in
place.
Outline a contingency plan if a patient refuses to cooperate or
demands to leave.
Outline management of a patient whose risk for suicide is chronic but
not imminent.
Discuss appropriate medications for patients at risk of suicide who
have a treatable psychiatric disorder.
Arrange for drug and alcohol counselling when appropriate.
Select patients in need of specialist assessment and treatment.
Inform and counsel family and friends.
426
109 Syncope I Pre-Syncope I Loss of Consciousness
Overview
Syncope is a transient, self-limiting loss of consciousness, usually leading to falling .
Syncopal episodes are common , accounting for 3-5% of attendances at emergency
departments and affecting 15- 25% of the population over a 10-year period. The
prevalence increases with age and syncope causes significant morbidity in the elderly.
Clinicians are requi red to distinguish syncope from seizures; and to distinguish syncope
caused by benign causes from syncope caused by serious underlying illness.
Causes
1) Neurally-medicated reflex syncopal syndromes
a) VasovagaVVasodepressorsyncope
b) Carotid sinus syncope
Carotid sinus syndrome (elderly subjects with vascular disease)
Situational faint (serious consequences may follow when confined
surroundings prevent falling)
0 Acute haemorrhage
0 Cough/Sneeze syncope
0 Gastrointestinal stimulation (defaecation, visceral pain)
0 Micturition
0 Post-exercise
0 Other (weightlifting, brass instrument playing, post-prandial)
c) Glossopharyngeal and trigeminal neuralgia
I 2) Orthostatic
a) Volume depletion
0 Haemorrhage
0 Diarrhoea
0 Addison disease
b) Vasodilator drugs (nitrates, antihypertensives, diuretics,
antidepressants)
c) Mechanical reduction of venous return
d) Autonomic failure
0 Primary autonomic fail ure syndromes (pure autonomic fai lure,
multiple system atrophy, Parkinson disease with autonomic failure)
0 Secondary autonomic failure syndromes (diabetic autonomic
neuropathy, amyloid neuropathy)
427
I 3) Cardiac arrhythmia
a) Sinus node dysfunction (including tachycardia/bradycardia
syndrome)
b) Atrioventricular conduction system disease
c) Paroxysmal supraventricular tachycardia
d) Paroxysmal ventricular tachycardia
e) Inherited syndromes (long QT, Brugada syndromes)
f) Implanted device malfunction (pacemaker, implantable cardiac
defibrillator (lCD))
g) Drug-induced (pro-arrhythmic drugs)
4) Structural cardiac or cardiopulmonary disease

a) Cardiac valvular disease (aortic stenosis, mitral stenosis, pulmonary
stenosis)
b) Acute myocardial infarction (MI) I ischaemia
c) Obstructive cardiomyopathy (hypertrophic cardiomyopathy)
d) Atrial myxoma
e) Acute aortic dissection
f) Pericardia! disease/tamponade
g) Pulmonary embolism
h) Pulmonary hypertension
i) Inflow obstruction (to systemic circulation)
I 5) Cerebrovascular causes
a) Vascular steal syndromes
Key Objectives
• Differentiate syncope from disturbances of cerebral function caused by a
seizure.
• Determine the severity of the complaint and categorise syncope according
to severity of underlying cause.
Differentiate between cardiac and non-cardiac causes.
Determine volume status.
428
Identify patients who require tilt table testing.
Diagnose disturbances of cardiac rhythm with the assistance of
electrocardiography (ECG) and Holter monitoring.
Select laboratory investigations most useful in assessment of volume
status and interpret the results.
• Conduct an effective plan of management for a patient with syncope I pre-
syncope I loss of consciousness:
Outline the plan of initial management.
List patients who may require cardiac pacing.
Evaluate patients for fitness to drive or work; be aware of Australian
guidelines.
Conduct counselling for patients with syncope.
429
110 Tall Stature I Short Stature I Abnormal Stature
Overview
To define any growth point, children should be measured accurately and each point
(height, weight, and head circumference) plotted. One of the more common causes of
abnormal growth is mismeasurement or aberrant plotting.
Causes
1) Tall stature (children develop pituitary gigantism;
adults are not taller, but have acromegaly)
a) Excess growth hormone (GH)
0 Pituitary adenoma (98%)
Extrapituitary tumour (very rare)
b) Excess GH releasing hormone secretion I growth factor activity
c) Other (Klinefelter syndrome, precocious puberty) -it should be
remembered that children with precocious puberty are tall at an early
age, but often finish up short due to premature bony fusion .
Acromegaly
12) Short stature

a) Intrinsic shortness (familial, Turner syndrome)
b) Delayed growth (constitutional, under-nutrition, underlying disease)
c) Attenuated growth
0 Chronic renal failure I Metabolic acidosis
0 Cancer I Chemotherapy I Glucocorticoid excess
Pulmonary/Cardiac/Gastrointestinal disease
0 Metabolic I Endocrine
• Vitamin D deficiency/resistance
• GH deficiency
430
• Hypothyroidism
• Cushing syndrome
0 Intra-uterine growth retardation (IUGR) (see #123 Weight (low) at
Birth I Intra-uterine Growth Aberration)
d) Accelerated early growth, more accelerated epiphyseal closure
(precocious puberty)
Key Objectives
• Determine whether growth progressively deviates from previously defined
percentiles.
• Determine whether the child has dysmorphic features.
Elicit history of uterine growth rate, intra-uterine infections, maternal
exposure to toxins, smoking, alcohol, or systemic illness.
Determine the presence of underlying medical problems (e.g. rickets,
hypothyroidism).
Calculate growth velocity, and relationship between chronological age,
height age, and bone age.
In a patient with tall stature, determine the presence of soft tissue
overgrowth (macrognathia, swollen hands and feet, nose, frontal
ridges).
Elicit information about joint symptoms (hypertrophic arthropathy),
headaches, visual problems.
Determine whether there is hypertension, left ventricular hypertrophy
(LVH), cardiomyopathy, cancer (gastrointestinal).
Select diagnostic imaging for bone age and for diagnosis of causes of
altered growth.
Screen for hormone disorders (particularly GH, thyroxine,
corticosteroid) and chromosomal abnormalities.
• Conduct an effective plan of management for a patient with abnormal
growth:
Counsel families and children with abnormal stature.
43 1
-
111 Tinnitus/Bruit
Overview
Although tinnitus is mostly harmless it is annoying and difficult to treat. The cause of
tinnitus in the vast majority of patients is idiopathic; in some it may be indicative of a
serious organic cause which may be reversible. A pulse-related auditory perception
suggests a vascular cause.
Causes
1) Auditory
a) Associated with sensorineural hearing loss
0 Presbycusis
Noise-associated
0 Meniere disease
CJ Neoplasms (acoustic neuroma, cerebellopontine tumour)
b) Drug-related
U Aspirin
Aminoglycosides
0 Other (chemotherapy, digitalis, quinidine)
c) Idiopathic
I2) Para-auditory
a) Pulse-synchronous
0 Vascular (carotid bruits, hyperdynamic states, aneurysm, venous
hum)
0 Glomus tumour
b) Non-pulse synchronous (temporomandibular joint (TMJ) dysfunction,
palatal myoclonus)
13) Psychogenic (anxiety, depression)
Key Objective
• Recognise that any condition of the ear associated with the ear canal
(wax, otitis media), cochlear hearing loss, or central nervous system (CNS)
hearing loss can cause tinnitus and the underlying cause must be
identified.
432
Determine whether or not the tinnitus is related to an ear condition or
hearing loss.
Determine whether the tinnitus is pulsatile or non-pulsatile (vascular
causes tend to be pulsatile).
Determine whether tinnitus is unilateral or bilateral.
Differentiate between drug-related causes, disease-related causes,
and tinnitus caused by noise.
Select patients for further investigation based on clinical findings .
• Conduct an effective plan of management for a patient with tinnitus:
Identify and counsel patients with causes of tinnitus which are benign.
112 Torticollis
(See #057 Involuntary Move ment Disorders I Tic Disorders)
433
113 Trauma/Accidents/Prevention
Overview
Trauma is the third most common cause of death worldwide - after cardiovascular
disease and cancer. Trauma is the leading cause of death in the age group under
45 years. Deaths from road accidents account for half of all trauma deaths in Australia.
Factors involved in motor vehicle deaths include speeding and alcohol; young males
contribute most significantly to this mortality. Additional costly morbidity results from
non-fatal road crash trauma.
Intense public awareness campaigns aim to decrease the hazards caused from alcohol
and other drugs, speeding fatigue and lack of restraints.
Management principles in traumatised patients are to:
• Check and rapidly restore vital functions (primary survey).
• Diagnose and manage the type and severity of specific injuries (secondary
survey).
• Complete rehabilitation after injury.
The level of care is matched to the patient's needs by effective triage.
Causes
Wounds and injuries range from trivial to catastrophic and wounding may be accidental
or intentional.
Major categories are:
1) Blunt trauma
a) Vehicle crash injuries
b) Closed bony and soft-tissue trauma from domestic, occupational,
sporting and other injuries
Hamstring 18Br - MRI
434
j 2) Penetrating trauma
a) Knives
b) Bullets
c) Lacerations and wounds from other causes
Key Objectives
• Match management to type and degree of trauma injury by efficient triage.
• Conduct an efficient primary and secondary survey of all traumatised
patients in accord with emergency management of severe trauma (EMST)
guidelines.
• Recognise and conduct an effective initial management plan for the
acutely traumatised patient.
• Conduct an effective and rapid primary survey ('ABCDE'):
Airway- establish patency and adequacy.
!iJ.reathing - check and evaluate breathing (look, feel , listen).
Circulation - assess for shock, control external bleeding, establish
intravenous access.
Disability- assess neurologic status, record Glasgow Coma Scale.
Exposure with temperature control -complete exposure and
examination which leads into secondary survey.
• Conduct an effective and rapid secondary survey through appropriately
focused data collection , while maintaining observations and imaging
relevant to primary survey:
Head and scalp.
Neck.
Thorax.
Abdomen and perineum.
Spine and extremities.
• Use appropriate diagnostic and management aids and adjuncts to primary
and secondary surveys appropriate to the type and degree of injury,
including:
Cardiopulmonary resuscitation (CPR), oxygenation, chin-lift and jaw
thrust, endotracheal intubation, cricothyroidotomy, needle and tube
thoracentesis, pericardiocentesis, tetanus prophylaxis, blood and urine
testing including blood cross match, intravenous access, urinary
catheterisation, pulse oximetry, plain X-ray, computed tomography (CT)
scan, contrast radiology.
435
113A Abdominal Injuries
Overview
Most abdominal injuries in Australia are blunt injuries associated with road crash
trauma. Penetrating injuries (e.g. knives, handguns) will usually require surgical
intervention. High velocity gunshot wounds are relatively uncommon but carry a
higher mortality and morbidity.
Causes
(see #113 Trauma/Accidents/Prevention)
!1) Blunt trauma
I 2) Penetrating trauma
Traumatic laceration of spleen
Key Objective
• Determine which injuries require surgical intervention and active
resuscitation .
See #113 Trauma/Accidents/Prevention for initial assessment and
resuscitative measures.
Determine whether significant blunt or penetrating abdominal injury
exists.
• Be aware of further investigations which may be required in management
(e.g. computed tomography (CT) scan).
• Conduct an effective initial plan of management for a patient with
abdominal trauma:
Outline the principles of management of abdominal trauma.
List indications for surgical consultation.
436
1138 Bone and Joint Injuries
(See also #041 Fractures I Dislocations)
Overview
Major fractures are often associated with other injuries, and priorities must be set for
each patient. Control of internal haemorrhage from a ruptured spleen takes precedence
over fracture management, but severely injured patients with open fractures should
have their fractures dealt with as soon as possible after admission to hospital, if
necessary by a combined specialty team. Management of many soft-tissue injuries is
facilitated by initial stabilisation of the bone or joint injuries.
Healing of fractures can be expected if the fragments have an adequate blood supply,
if the bone surfaces are apposed without soft tissue interposition and if immobilisation
of the fracture is adequate. Defective local conditions are far more potent sources of
delayed union than are systemic or host facrors.
Fracture neck of humerus Intertrochanteric fracture right femur
Causes
1) Varieties of bony injuries
a) Complete/Incomplete ('greenstick') fractures
b) Open/Closed injuries
c) Displaced/ Undisplaced/Stable/Unstable fractures
437
I 2) Mechanisms of injury
a) Direct violence (transverse, oblique, 'butterfly', comminuted
fractures)
b) Indirect violence (spiral, compression, avulsion fractures)
Fracture clavicle
Colles fracture
Key Objectives
• Recognise principles of management as fracture/dislocation reduction
with restoration of normal alignment and length, retention until healing
occurs, rapid restoration of function, and effective rehabilitation .
• Recognition that methods of management used vary according to
circumstances between: no immobilisation except a supportive sling,
closed reduction and plaster cast immobilisation; closed reduction and
continuous traction; external skeletal fixation devices; operative reduction
and internal fixation.
438
113C Burn Injuries
(See # 018 Burns)
Superficial bums of back (healing eschar)
1130 Chest Injuries
Overview
Injury to the chest may be blunt (e.g. motor vehicle trauma, falls, blast and crush
injuries) or sharp (knife or bullet). Management of open sucking wounds and of
pneumothorax will often need urgent intervention to maintain breathing and adequate
oxygenation. Imaging and other diagnostic investigations may need to be delayed
until the patient has been resuscitated and stabilised.
Causes
!1) Chest wall/ Lung

Respiratory Disese: With Pleural Chest X-Ray Abnormality)
a) Flail chest
b) Haemothorax
c) Pneumothorax (open, closed)
d) Rib fracture
I 2) Heart injury
a) Pericardia! trauma (pericarditis, acute/delayed tamponade,
constrictive pericarditis)
b) Myocardial trauma (contusion, coronary vessel injury, traumatic
valve injury)
c) Aortic rupture
439
Key Objective
• Appreciate that patients with chest injuries frequently present with shock or
with respiratory compromise. Diagnosis and appropriate emergency
treatment depends on suspicion and diagnostic acumen.
Differentiate between hypotension I shock from bleeding and from
tamponade.
Appreciate that aortic rupture may be present (chest or mid-scapular
pain, dyspnoea, hoarseness, dysphagia) although it may be
asymptomatic.
In patients with lung contusion after blunt injury to the chest, or massive
traumatic tissue injury, examine lungs for oedema from acute
respiratory distress syndrome.
Select diagnostic imaging of the chest as indispensable for accurate
diagnosis.
• Conduct an effective initial plan of management for a patient with chest
trauma:
Select patients in need of specialised care in an intensive care unit
(ICU).
440
113 Trauma/ Accidents/Prevention
113E Cold Injuries
(See #040D Hypothermia)
113F Eye Injuries
(See also # 120 Visual Disturbance/Loss)
Overview
Eye injuries are common. Fortunately the blink reflex and Bell reflex (turning the eyes
upward when the lids close) usually protect the globe from blunt trauma. Emergency
assessment should check systematically vision, orbital surrounds, lids and eyebrows,
and ocular movements. The globe is assessed for lacerating/abrading injury and
foreign bodies inspecting sclera/conjunctiva, cornea, pupil size, shape and reaction ,
iris, and anterior and posterior chambers by direct ophthalmoscopy. Chemical eye
burns will require immediate and copious aqueous irrigation. Most uncomplicated
'black eye' injuries will resolve spontaneously with cold compresses. Restricted eye
mobility may indicate entrapment of extraocular muscles in a blowout fracture requiring
surgery. Penetrating eye injuries require immediate specialist referral.
Causes
j1) Blunt trauma
I2) Burn injuries
I3) Penetrating trauma
Key Objectives
• Ability to assess from history and examination the result of injury, checking
systematically vision, orbital surrounds, lids and eyebrows, and ocular
movements.
• Abil ity to recognise serious injuries threatening sight.
441
113G Facial Injuries
Overview
Facial injuries are potentially life-threatenin g because of possible damage to the
airway and central nervous system (CNS).
Causes
l1) Blunt injuries
12) Penetrating (open) injuries
Key Objective
• Assess and control vital functions and give management priority to life-
threatening injuries. Definitive treatment of the facial injury is relatively less
urgent, but of major cosmetic importance.
Elicit a history about the nature of the injury.
Evaluate airway, cardiopulmonary and neurologic status.
List the most appropriate investigations used to determine the nature
and severity of facial injuries.
• Conduct an effective initial plan of management for a patient with facial
injury:
Outline the priorities in the management of a patient with a facial injury.
Outline and provide the initial management of patients with facial
injuries.
List indications for specialised care.
442
113H Hand/Wrist Injuries
Overview
Hand and wrist injuries are common
problems presenting to emergency
departments. The ultimate function of the
hand depends upon the quality of the initial
care and the severity of the original injury.
Causes
Hand injuries commonly follow injuries
associated with occupational, domestic,
sporting and other recreational activities.
Scaphoid fracture
Key Objective
• Demonstrate the assessment of the nature and extent of hand injuries.
Appreciate the differing mechanisms of injury.
Appreciate the distinction between 'tidy' and 'untidy' hand injuries.
Elicit history of antecedent trauma and type, and assess the nature and
extent of injury. Diagnose damage to tendons, nerves, bones and
joints, skin and soft tissues.
Determine active and passive range of motion, inspect and palpate
joints for deformity, and differentiate between radial , ulnar, and median
nerve sensory and motor deficit.
Select patients whose trauma suggests risk of fractures for radiographs
of the affected bones and joints.
• Conduct an effective initial plan of management for a patient with a hand
injury:
Outline initial management for injuries of the hand/wrist.
Select patients in need of splints, conservative management, referral
for occupational or physiotherapy, or surgery.
-.44 3
1131 Head Injuries

(See #045 Head Injuries I Brain Death I Transplant Donation and
#104 Spinal Injuries)
113J Nerve Injuries
Overview
As a component of major injury, damage to peripheral nerves may go unrecognised.
Accurate assessment of motor and sensory function of a limb involved in injury is
essential.
Causes
11) Compression/Stretch
I2) Contusion
I3) Laceration/Division
Key Objective
• Identify the peripheral nerve involved, the level and type of involvement.
Elicit and interpret information from the history and physical
examination to distinguish a peripheral nerve injury from other non-
traumatic neuropathies or central lesions.
Differentiate between injuries causing neurapraxia, axonotmesis, and
neurotmesis.
Outline the methods used to diagnose the presence of a traumatic
peripheral neuropathy.
• Conduct an effective initial plan of management for a patient with nerve
injury:
444
113K Skin Injuries
Overview
Wounds are open injuries of tissue. The morbidity associated with skin wounds is
determined by the severity and site of the injury and the overall state of health of the
patient. Severity of skin wounds depends on the extent of penetrating and disrupting
skin and soft tissue injury, and of the degree and duration of bacterial contamination
prior to treatment. Many skin and subcutaneous wounds are superficial and can be
repaired under local anaesthesia. Differentiation between 'tidy' and 'untidy' wounds
is crucial to management.
Causes
1) 'Tidy' wounds (e.g. sharply-incised and penetrating wounds,
damage restricted to wound path, contamination minimal and
brief)
2) 'Untidy' wounds (e.g. lacerations, high-velocity missile wounds,

widespread tissue damage, contamination severe and prolonged).
Examples include avulsions, bites and crush injuries as well as
gunshot and missile wounds
Key Objectives
• Prior to wound closure, examine all patients thoroughly for evidence for
injuries involving important underlying structures (tendon, nerve, vessel).
• Appreciate principles of adequate wound debridement for traumatic
wounds.
• Appreciate principles of infection prophylaxis, including recognition and
treatment of tetanus-prone wounds.
Elicit and interpret information from history and physical examination to
determine the nature and severity of the skin wound, time since injury
(more than 24 hours or less than 24 hours), presence of infection.
In all cases of human bites, elicit information about HIV status, hepatitis
status.
Select patients whose HIV and hepatitis status requires investigation.
445
• Conduct an effective initial plan of management for a patient with skin
injury:
Provide definitive care of superficial wounds involving the skin and
subcutaneous tissues.
Identify wounds that require specialised care; list indications for
specialised care.
Discuss prophylaxis to prevent infection.
Outline principles of wound management.
List indications and contraindications of primary versus delayed
closure.
Select the appropriate suture material and closure technique.
Outline management of a human bite if the assailant is HIV/hepatitis
positive; if the puncture is caused by a syringe needle or contaminated
knife.
448
113L Spinal Injuries
(See # 104 Spinal Injuries)
113M Urinary Tract Injuries
Overview
Closed injuries of the urinary tract are more common than penetrating injuries. Injuries
are classified into kidney injuries, ureteric injuries, and bladder and urethral injuries.
Pelvic fractures - possible bladder/urethral I
Causes
1) Kidney injuries - associated rib fractures are common from
motor vehicle injuries, falls, sporting injuries and blows
2) Ureteric injuries (surgical division or injury)
I 3) Bladder and urethra

a) Bladder and posterior (prostatomembranous) urethra- associated
with pelvic fracture or abdominal injury. Full bladder at time of injury
increases risk of intraperitoneal or extraperitoneal bladder rupture
b) Anterior urethra- associated with falls astride, kicks to perineum and
instrumental damage
Key Objectives
• Early recognition and treatment of kidney injuries aided by urine
examination and imaging.
447
• Rupture of bladder or posterior urethra must always be suspected in
patients with pelvic fractures.
• Recognition that bleeding occurring at the external urethral meatus after
injury is the cardinal sign of urethral injury and requires urgent ascending
urethrography.
Select computed tomography (CT) scanning with intravenous contrast
as appropriate investigation for renal injury.
Identify patients with renal injury requiring early angiography imaging.
Select ascending urethrogram as appropriate initial investigation for
urethral injury.
Outline diagnostic and management plans for suspected urinary injury.
Recognise urinary injuries early and categorise into renal, ureteric or
urethral injuries.
Recognise haematuria (macroscopic or microscopic), bleeding from
urethral meatus and inability to void as important diagnostic features.
Select computed tomography (CT) scanning with intravenous contrast as
appropriate investigation for renal injury.
Identify patients with renal injury requiring early angiography imaging.
Select ascending urethrogram as appropriate initial investigation for
urethral injury.
Outline diagnostic and management plans for suspected urinary injury.
448
113N Vascular Injuries
Overview
Vascular injuries of blunt trauma often involve vessels near joints (e.g. knee, elbow)
where vessels are relatively fixed and vulnerable to the shearing forces of fractures
and dislocations. Complete or partial transection of the vessel can result in significant
local haematoma; alternatively, throm bosis may be due to intimal rupture and elastic
recoil without significant blood loss. Penetrating vascular injuries result usually from
stab, gunshot or other missile wounds and are more likely to involve segmental loss of
artery and vein , especially with high-velocity missile injuries. Although haemorrhage,
haematoma, a pulse deficit and distal ischaemia are cardinal signs of vascular injury,
a high index of suspicion is required as, in nearly one-third of patients with penetrating
arterial injuries of limbs, signs of distal ischaemia are absent and distal pulses are
palpable.
Common Causes of Vascular Injury

1) Closed injury (e.g. motor vehicle accidents (MVA))
a) Head and neck injuries (epidural haemorrhage, carotid occlusion)
b) Supracondylar humeral fracture, fracture/dislocation of the elbow
(brachial artery occlusion)
c) Fractured pelvis (major iliac venous and arterial bleeding)
d) Closed chest injuries (aortic tear)
e) Supracondylar femoral fracture, dislocated knee (popliteal artery
occlusion)
f) Hyperextension lumbar spine injuries (renal arteries)
2) Open injury (penetrating knife or gunshot wounds of neck,

abdomen, groin, iatrogenic injury)
Key Objectives
• Diagnose major vascular injuries early by appropriate assessment and
high index of suspicion.
• Provide initial management and obtain consultation when indicated.
• Classify whether injury is occlusive or haemorrhagic with open vessel.
449
examination to diagnose an arterial injury.
examination to diagnose compartment syndromes.
• Interpret critical clinical and laboratory findings (ultrasound, imaging with
and without contrast, haematology and biochemistry) which were key in
the processes of exclusion, differentiation, and diagnosis:
List the most appropriate investigations used in the diagnosis of
vascular injury.
• Conduct an effective and rapid initial plan of management for a patient
with vascular injury:
List risks in the use of tourniquets and clamps.
Outline the initial management of arterial injuries.
450
114 Urinary Frequency
114A Urinary Frequency: Associated with 1Dysuria and/

or Pyuria 1 Urethral Discharge'
Overview
Patients with urinary tract infections (UTis), especially the very young and the very old,
may present in an atypical manner. Appropriate diagnosis and management may
prevent significant morbidity. Dysuria can mean either pain on micturition or difficulty
with micturition. Pain usually implies infection and difficulty is usually related to
mechanical obstruction at some point distal to the bladder neck, most commonly from
prostatic enlargement.
Causes
1) Urinary frequency (volume greater than 2 ml/minute)
2) Urinary frequency (normal or decreased volume) associated with

dysuria and/or pyuria
a) Externai to urinary tract (infectious vulvovaginitis, colovesical fistula)
b) Irritable bladder (psychogenic)
c) Urinary tract involved
0 Urethritis (e.g. gonococci, acute urethra syndrome, Trichomonas)
0 Prostatitis
UTis
• Cystitis
• Pyelonephriti s
Ureteric reflux - MCU Duplex system
451
Key Objectives
• Differentiate between UTis and conditions outside the urinary tract with
similar presentation; determine which infections requ ire treatment, and
select the appropriate treatment.
• Consider factors predisposing to infection in patient with recurring UTis
(obstruction and stasis, calcu li, reflux) .
Interpret urinalysis and clinical findings in order to diagnose problems
external to urinary tract.
Evaluate examination fi ndings so that problems involving the urethra or
prostate are identified.
Determine whether cystitis or pyelonephritis is the more likely
diagnosis.
Outline significance of patient's age, gender, and lifestyle on diagnostic
possibilities.
State or select findings which are best for differentiating cystitis from
pyelonephritis.
Describe the collection of samples to be sent for culture and sensitivity;
state their interpretation.
• Conduct an effective plan of management for a patient with urinary
frequency associated with dysuria and/or pyuria:
Determine which patients require additional investigation and/or
referral.
Determine which patients require hospitalisation.
Determine which patients should be on prophylactic treatment and the
type of treatment.
Select the most appropriate treatment for the underlying condition.
List conditions which predispose to UTis.
Outline strategies for prevention of recurrent UTis.
452
114 Urinary Frequency
1148 Urinary Frequency: Associated with 1Polyuria/

Polydipsia'
Overview
Urinary frequency, a common complaint, can be confused with polyuria. a less common ,
but important complaint. Diabetes mellitus is a common disorder with morbidity and
mortality that can be reduced by preventive measures. Intensive glycaemic control
during pregnancy will reduce neonatal complications.
Causes
1) Urina ry fre que n c y (volume g r e ater than 2 ml/minute )

a) Water diuresis
.J Polydipsia
u Diabetes insipidus (central or nephrogenic)
b) Osmotic diuresis
...J Diabetes mellitus
U Chronic renal disease
2) Urinary fre que ncy (norma l or d ecre a sed volume ) associate d with
dys uria and/or pyuria
Note: Decreased bladder capacity may produce no symptoms apart from urinary
freq uency.
Key Objective
• Evaluate diabetic patients and determine whether diabetic ketoacidosis or
hypoglycaemia is present; formulate a management plan for diabetic
emergencies.
(see #053 Hyperglycaemia I Diabetes Mellitus)
Differentiate urinary frequency from polyuria.
Contrast water diuresis and osmotic diuresis.
Select and interpret laboratory tests which distinguish between water
and osmotic diuresis.
• Conduct an effective plan of management for a patient with polyuria/
polydipsia:
453
115 Urinary Incontinence I Enuresis
115A Urinary Incontinence, Paediatric Enuresis
Overview
Enuresis is the involuntary passage of urine into bedclothes or undergarments. At
least 90% of presenting children will have primary nocturnal enuresis. Diurnal and
secondary enuresis is much less common , but requires differentiating between
underlying organic diseases and stress-related conditions.
Causes
1) Primary enuresis
a) Idiopathic/Familial
b) Anatomic abnormality
I 2) Secondary enuresis
a) Urinary tract infection (UTI)
b) Diabetes mellitus/insipidus I Primary polydipsia
c) Neurologic disorder
d) Psychogenic I Stress
Key Objective
• In a child five years of age or older, determine whether a physical
abnormality is causing the involuntary passage of urine.
Determine whether medical reasons underlie the enuresis.
Determine whether a stressful event preceded the occurrence of
enuresis.
Select patients who require investigation.
• Conduct an effective plan of management for a patient with acute enuresis:
Counsel, educate and reassure the parents of a child with primary
nocturnal enuresis.
In a child with primary enuresis, discuss treatment options including
family education and observation of the problem, reward systems,
behavioural strategies, conditioning alarm system, medication
(1-desamino-BD-arginine vasopressin (DDAVP), imipramine).
In a child with secondary enuresis, outline a management plan to treat
the underlying cause.
454
115 Urinary Incontinence I Enuresis
1158 Urinary Incontinence, Elderly
Overview
Because there is increasing incidence of involuntary micturition with age, incontinence
will increase in frequency as our population continues to age.
Causes
1) Stress incontinence
a) Women after the menopause when oestrogen deficient (especially
multiparae)
b) Post hysterectomy I Prostatectomy
c) Bladder tumour
2) Urgency incontinence
a) Cystitis, urethritis
b) Vesical polyps, carcinoma, stones
c) Psychogenic
d) Dementia
3) Reflex incontinence
a) Spinal transverse paralysis above T12
b) Spinal tumour
c) Syringomyelia
4) Overflow incontinence
a) Prostatic obstruction
b) Urethral stricture
c) Diabetes mellitus
d) Multiple sclerosis
5) True incontinence - urinary fistulas (including postoperative)
Key Objective
• Contrast between the two most common causes of incontinence, stress
incontinence and urgency incontinence (insufficient sphincter closure in
stress incontinence versus excessive detrusor contraction with urgency).
455
Differentiate between stress, urgency, reflex, and overflow and true
incontinence, especially in the female .
Perform a pelvic examination and rectal examination for prostate size
in the male.
Perform urinalysis.
Select patients in need of cystoscopy and other specialised tests such
as urodynamic studies.
• Conduct an effective plan of management for an elderly patient with
urinary incontinence:
Outline a plan of management for cystitis and urethritis.
Counsel patients with stress incontinence I urge incontinence.
Select patients in need of referral for urodynamic studies,
physiotherapy or surgical treatment.
456
116 Urinary Obstruction I Hesitancy I Prostatic
Cancer I Screening
Overview
Urinary tract obstruction, either upper or lower tract, is a relatively common problem.
The obstruction may be complete or incomplete. The most common cause in an elderly
male is prostatomegalic. Obstruction may be unilateral in the upper tract and
asymptomatic. The consequences of the obstruction depend on its onset, nature and
overall renal function.
Prostate cancer is usually found in older men (median age at diagnosis is 71 years).
One in ten Australian males may develop prostatic cancer at some stage of life; as the
growth pattern is usually slow, perhaps one in 50 males will die from , rather than with ,
prostatic cancer.
Metastatic prostate cancer
Causes
1) Child (anatomic abnormalities)
a) Urethra (stricture, valve)
b) Junctions (ureterovesical, ureteropelvic)
12) Adult (calculi)
457
13) Elderly
a) Prostatomegaly
(benign hyperplasia, cancer)
b) Calculi
c) Retroperitoneal neoplasm
d) Pelvic neoplasm
Key Objectives
• Determine the site and duration of the obstruction.
• Determine when acute obstruction requires urgent management.
Determine whether the obstruction is acute or chronic, complete or
partial, and unilateral or bilateral.
Select ultrasonography as the diagnostic imaging tool to diagnose
obstruction.
List indications for other types of diagnostic imaging.
Select and interpret tests of renal function.
• Conduct an effective plan of management for a patient with urinary tract
obstruction:
Perform catheterisation of the bladder for both therapeutic and
diagnostic reasons.
Select patients for referral to specialised care.
• Discuss methods, advantages and disadvantages of screening for
prostatic cancer.
458
117 Vaginal Bleeding, Excessive in Amount or Irregular
in Timing
Overview
Vaginal bleeding is considered abnormal when it occurs at an unexpected time (before
menarche or after menopause) or when it varies from the norm in amount or pattern.
Causes
1) Not related to pregnancy - gynaecologic
a) Hypothalamic-pituitary-ovarian dysfunction
0 Anovulatory/Ovulatory
0 Functioning ovarian cysts/tumours
0 Emotional stress, drugs, hormones, oral contraceptives
b) Outflow tract conditions
0 Uterus (infection, trauma, cancer/benign masses)
0 Cervix (cervicitis, trauma, carcinoma)
0 Vagina/Vulva (infection, trauma, cancer)
2) Related to pregnancy - non-gynaecologic

a) less than 20 weeks
0 Miscarriage-threatened, inevitable, incomplete, complete, missed,
septic
0 Ectopic pregnancy
0 Gestational trophoblastic disease
b) Twenty weeks
0 Placental abruption
0 Placenta praevia
0 Incidental bleeding - i.e. non-pregnancy causes which occur in
pregnancy
0 Bleeding from a vasa praevia - fetal bleeding
Key Objectives
• Determine whether the patient is haemodynamically stable prior to any
other task.
• State that history is important, but diagnosis depends on hormonal/
cytologic studies.
• Determine the difference between pregnancy related and non-pregnancy
related causes.
459
First differentiate between bleeding related to or unrelated to
pregnancy.
If age or clinical information makes pregnancy unlikely, differentiate
between causes of gynaecologic bleeding.
State that pelvic examination is not indicated in a woman more than
20 weeks pregnant with bleeding until ultrasou nd has been performed
and excluded placenta praevia.
Perform pelvic and rectal examination.
List indications for hormonal studies, and select tests.
List indications for ultrasonog raphy.
List indications for cytologic/biopsy studies and select patients to be
referred for investigation.
• Conduct an effective plan of management for a patient with vaginal
bleeding:
Outline management of patient with threatened and other forms of
miscarriage.
Outline followup of patient after treatment of ectopic pregnancy;
gestational trophoblastic disease.
Where sexual abuse is suspected, outline legal implications and
requirement for support.
Discuss the use of oral contraceptives for regulating hypothalamic-
pituitary-ovarian dysfunction.
480
118 Vaginal Discharge I Urinary Symptoms, Vulvar
Lesions, Sexually Transmitted Diseases (STDs)
Overview
Vaginal discharge, with or without pruritus, is one of the most common problems seen
in the clinician's office.
Causes
1) Physiologic discharge, and cervical mucus production
2) Genital tract infections - vulvovagi nitis - infectious

a) Polymicrobial superficial infection
b) Moniliasis (candidiasis)
c) Trichomoniasis
d) Bacterial vaginosis
e) Human papilloma virus (HPV)
f) Herpes genitalis
Anovulval warts
461
3) Genital tract inflammations - vulvovaginitis - noninfectious
a) Bubble baths, chemical irritants, douches, sprays
b) Foreign body
c) Atrophic vaginitis I Atroph ic or hypertrophic vulvar dystrophy
d) Vulvar intraepithelial neoplasia I Vaginal, genital neoplasia
e) Systemic process (toxic shock syndrome)
4) Other genital tract causes - uterine and tubal

a) Infections
0 Gonorrhoea and Chlamydia
0 Intra-uterine device
0 Pyosalpinx
0 Salpingitis
b) Vu lval, cervical, endometrial and tubal neoplasia
..
5) Desquamative inflammatory vaginitis I Focal vulvitis
Key Objectives
• Determine the appearance of the discharge, but state that appearance
may be misleading, and up to 20% of patients may have two coexistent
infections.
• Differentiate between urinary tract infections (UTis) and vaginal infections
(dysuria is a symptom of both, so determine whether vaginal discharge is
present).
• Define the cause of the discharge - whether inflammatory or neoplastic,
and site within the genital tract.
462
Differentiate between 'external' and 'internal' dysuria.
Elicit information about precipitating or aggravating factors (oral
contraceptives, antibiotics, pregnancy, sexual activity, diabetes, genital
hygiene, chemical irritants, etc.).
Perform genital and pelvic examination; determine whether pelvic
inflammatory disease is present.
Contrast pH and wet or potassium hydroxide smear findings in vaginitis
of yeast, bacterial, Trichomonas, or atrophic type.
Select patients with purulent discharge for a Gram stain and cervical
culture.
Perform Papanicolaou (Pap) smear to evaluate cervix (may also pick
up carcinoma of the endometrium or tube).
• Conduct an effective plan of management for a patient with vaginal
discharge:
List screening of populations at high risk for sexually transmitted
diseases (STDs).
List types of vulvovaginitis associated with sexual activity and discuss
risk reduction.
Outline preventive measures for STDs (e.g. limiting number of sexual
partners, barrier contraceptives, especially condoms) ; for prevention of
noninfectious vaginitis.
Outline a management plan for moniliasis, trichomoniasis, and for
vaginitis due to gonorrhoea and/or Chlamydia including role of local
hygiene in prevention.
483
119 Violence/ Aggression and Mental Illness
Overview
Aggression is any form of behaviour intended to harm or injure other people against
their wishes. Violence is a deliberate attempt to inflict physical harm. Dangerousness
refers to the likelihood of whether individuals present a risk of harming themselves or
others. Clinicians are confronted with the direct and indirect consequences of violent
behaviour and will be increasingly expected to make risk assessments of future
dangerousness. Although comorbidity of some mental illnesses increases the risk of
violence , most episodes of violence are not committed by mentally ill people. T he best
predictor of future violence is past violence, but violent behaviour is usually the result
of the interaction of many factors.
Predisposing Causal Factors

1) Pre-existing vulnerabilities (gender, age, personality, impulsivity,
intellectual functioning, neurobiology, individual sensitivity,
conduct disorder, family and cultural influences)
I 2) Psychiatric disorders
a) Schizophrenia (with active paranoid, or grandiose ideation or
command hallucinations, treatment resistance and impaired insight)
b) Delusional disorder (particularly morbid jealousy)
c) Substance abuse (intoxication, withdrawal)
d) Major depression with delusions
e) Personality disorder (antisocial, borderline, conduct disorder)
f) Intermittent explosive disorder
g) Bipolar affective disorder (manic phase)
h) Cognitive disorders (delirium, dementia)
3) Situational triggers (loss, actual or threatened; confrontation;

availability of weapons and presence of a potential victim)
Key Objectives
• List risk factors for dangerousness.
• Recognise signs of imminent violence: threats, paranoid ideas, shouting
and pacing, agitated behaviour.
464
• Through efficient, focused and tactful data gathering:
Elicit a history of violence in the distant and recent past, violence
against animals and property, forensic history, current thoughts or
threats of violence against named victims; degree of insight and ability
to maintain control.
Assess and document mental state for cognitive, intellectual and
psychotic features and degree of intoxication.
Determine presence of support systems and recent stressors.
Determine the ability and willingness to cooperate with management.
• Conduct an effective plan of management for a patient who may be violent:
Outline how to conduct the initial interview with an agitated and
potentially violent patient.
Outline a safe psychopharmacological management strategy for
treating a violent patient.
Understand clinician's responsibility to warn police or potential victims
in contrast to strict doctor-patient confidentiality.
Select patients in need of specialist referral and treatment.
Provide counselling and debriefing to victims and onlookers in the
aftermath of an episode of violence.
48!
119 Violence/ Aggression and Mental Illness
119A Child Abuse
Overview
Child abuse is part of the spectrum of family dysfunction and leads to significant
morbidity and mortality (recently, sexual attacks on children by groups of other children
have increased). Abuse causes physical and emotional trauma, and may present
as neglect. The possibility of abuse must be in the mind of all those involved in
the care of children who have suffered traumatic injury or have psychological or
social disturbances (e.g. aggressive behaviour, stress disorder, depressive disorder,
substance abuse).
Causes
(see #11 9 Violence/Aggression and Mental Illness)
Types of Abuse:
1) Physical abuse (pushing, hitting, biting, burning, locking out of

home, abandoning in an unsafe place)
2) Sexual abuse (forced unwanted sexual activity: rape, sex with

objects, friends, animals, mimic pornography, wear more
provocative clothes, etc.)
3) Emotional or psychological abuse (constant criticism; threats to

hurt, kill; extreme jealousy; denying friendships, outside
interests or activities; time accounting, etc.)
4) Economic (not allowing money, deny improvement in earning

capacity, accounting of every cent, etc.)
5) Other
a) Munchausen syndrome by proxy
b) By nurses, medical practitioners, social workers
Key Objective
• Identify the characteristics of families at risk of abusing their children
(physical, sexual or emotional abuse) and screen.
466
Determine the family dynamics, and parental characteristics.
Differentiate abuse by commission from abuse by omission.
Determine social correlation.
Determine whether the child has signs of physical, sexual, or other
abuse (e.g. cutaneous markings, burns), or emotional and
behavioural signs of abuse.
List investigation for a child with sexual abuse.
• Conduct an effective initial plan of management for a child who may have
been abused:
Outline strategies for securing the child's safety.
List indications for reporting to appropriate social service department or
referral to child welfare.
List potential physical and psychological sequelae of physical and
sexual abuse.
Outline treatment options for victims and perpetrators and outline
outcomes of treatment.
Outline strategies for prevention of child abuse.
487
119 Violence/Aggression and Mental Illness
1198 Elder Abuse
Overview
The American Medical Association defines elder abuse ('granny battering') as:
'an act or omission that results in harm or th reatened harm to the health or welfare of an
elderly person. Abuse includes intentional infliction of physical or medical injury; sexual
abuse; or the withholding of necessary food , clothing and medical care to meet the physical
and mental needs of an elderly person by one having the care, custody or responsibility for
an elderly person'.
There are no reliable estimates on the incidence or prevalence of elder abuse in

Australia, but international experience suggests that about 1 in every 25 elderly may
be victims, with only one in five cases reported. The typical victi m is an increasingly
dependent, cognitively impaired woman, over 75 years, with problem behaviours
including shouting and wandering. The typical abuser is a close relative in a long term
relationship (spouse or child) , who is under increasing stress, socially isolated and
abusing alcohol or drugs. There is no provision for mandatory reporting of elder
abuse in Australia.
Causes (Frequently in Combination)

1) Physical dependency
2) Caregiver stress
3) Pattern of family violence
4) Pathological alcohol/drug abuse
Types of Abuse:
1) Physical/Sexual
2) Emotional/Psychological
3) Medical
4) Economic exploitation
5) Neglect
Key Objective
• Identify both abused elderly patients and those at risk of abuse; and
differentiate abuse from organic brain disorders and dementia.
468
• Through efficient, focused data gathering which involves talking to both the
alleged victim and the caregiver separately:
Determine whether the explanations for illnesses or injuries are
consistent or implausible. Denial may be the initial response.
Conduct a thorough physical examination of the patient and document
bruises, bites, burns, lacerations and other injuries present, especially
in areas usually covered by clothing and on the scalp.
Determine the period of time between the injury and accessing the
medical system, since long delays are usual with elder abuse.
• Develop an effective initial plan of management for an elderly person who
may have been abused, which may involve initial hospitalisation, respite
care or long term alternative accommodation if there is concern for the
patient's physical health or safety:
Understand the legal implications of elder abuse.
Counsel and help caregiver by providing information and education
and accessing community options.
Outline the multidisciplinary approach to intervention and become
aware of local resources.
469
119C Violence: Domestic/Family
Overview
Domestic and family violence are major public health concerns which affect about
three percent of the Australian population annually. They can affect anyone irrespective
of economic, social, geographic or racial background, resulting in significant morbidity
and mortality. From a health perspective, domestic violence is a chron ic syndrome
characterised not only by physical violence, but also by emotional and psychological
abuse. It is the abuse of power in a relationship involving domination , coercion ,
intimidation and the victimisation of cv·.. .: person by another, typically a male partner.
Women are eight times more likely to be victims than males. The perpetrators are
often young, troubled, unemployed men with low self-esteem, who have been abused
themselves. Shame and isolation militate against disclosure, but health professionals
have responsibility to break the silence. Depression and post-traumatic stress disorder
are common sequelae for victims, as are alcohol and drug abuse, self-harm and
suicide. Barriers to disclosure often lie with the clinician and not the victim. Programmes
for stopping domestic violence can be effective for those who are motivated to change
their behaviour.
Classification of Domestic/Family Violence

1) Physical: resulting in pain, injury, denial of sleep, warmth or
nutrition, denial of medical care, violence to animals and
property, disablement and murder: dowry and honour killings
2) Sexual: coerced sex, rape, harassment, incest, pornography
3) Verbal: designed to humiliate, degrade, demean, intimidate,

subjugate, including the threat of physical violence
4) Economic: deprivation of basic necessities, seizure of income or

assets, unreasonable denial of the means to participate in social
life
5) Social: isolation, control of social activity, deprivation of liberty

or the deliberate creation of unreasonable dependence
470
Key Objectives
• Recognise the typical symptoms and signs, both physical and
psychological, which may indicate domestic violence.
• Assess immediate and short term risks to the victim.
• Know the common myths about domestic violence, namely that it is rare,
and only involves physical violence; that the perpetrators are mentally ill
and cannot control their anger and are always provoked by their victims;
that it is a problem only amongst the disadvantaged and minority groups
and that it is a private matter between individuals.
• Through efficient, sensitive and focused data gathering:
Include enquiries about possible domestic violence when patients
present with obvious physical injuries and bruising in multiple areas or
the head and neck; with chronic pain syndromes; insomnia,
depression, suicidal ideation; panic/anxiety; eating disorders; drug and
alcohol abuse, somatoform disorders; and also during pregnancy and
childbirth associated with unwanted pregnancy, miscarriage;
antepartum haemorrhage; avoidance of antenatal care or low infant
birthweight.
Consider the possibility in women with a past history of child abuse or
a child who is currently being abused; who have recently undergone
separation or divorce; who are socially isolated; who present frequently
or with an overly attentive partner; who delay in seeking treatment for
injuries or who do not comply with treatment.
Be aware that women who have been abused want to be asked about
domestic violence and are more likely to disclose if asked. Most
women do not openly admit they are victims of abuse unless asked:
out of fear, shame, denial, loyalty to their partner and family, or that they
will not be believed.
Document history, extent and type of abuse and injuries in detail and
provide appropriate treatment.
Assess the victim's immediate and short term safety and establish if the
perpetrator has a gun or other weapon at home.
Implement an effective plan of management for a victim of domestic
violence which may include supportive and educational counselling
and the provision of information about support services and resources
and sexual assault centres.
471
Assist in devising a safety plan in advance for a worst-case scenario.
Establish presence and attitudes of other potential support persons
towards the victim.
Refer patients for legal and police advice if necessary.
Select patients in need of specialist referral for social work,
psychological or psychiatric counselling.
If the victim and perpetrator are both your patients, issues of
confidentiality and disclosure arise.
Respect the patient's autonomy and right to remain in an abusive
relationship, even if you do not agree.
Remember that doctors are obliged to report situations where children
are at risk of violence or abuse.
1190 Rape I Violence Against Women
(See #119C Violence: Domestic/Family)
472
120 Visual Disturbance/Loss
Overview
Loss of vision is a frightening symptom that demands immediate attention, particularly
if acute. However, patients with neurological lesions may not be aware of visual loss;
and patients with a pituitary adenoma rarely present with symptoms of visual loss.
Causes
Acute:
11) Corneal (oedema)
I 2) Glaucoma (acute angle closure)
3) Vitreous haemorrhage (may be traumatic, penetrating, hyphaema)
4) Retinal/ Macular I Optic disc problems

a) Acute macular lesion
b) Retinal detachment (may be traumatic)
c) Retinal artery occlusion
d) Optic neuritis
e) Amaurosis fugax
f) Anterior ischaemic optic neuropathy
I 5) Nervous system
a) Occipital infarction/haemorrhage
b) Functional visual loss
I 6) Migraine
(see #046 Headache)
473
Chronic:
1) Corneal disorders (dystrophy, scarring, oedema)
Cataract left eye
2) Lens disorders (age related, traumatic, steroid-induced, ultra

violet light exposure)
3) Glaucoma (primary, secondary)
4) Ret inal dysfunction

a) Diabetic (retinal oedema, retinopathy)
b) Vascular insufficiency
c) Tumours
d) Macular degeneration or dystrophy
474
I
5) Optic nerve lesions
a) Compressive optic neuropathy
0 Intracranial (masses)
0 Orbital (thyroid disease)
b) Toxic/Nutritional (nutritional deficiencies, tobacco-alcohol amblyopia,
methanol)
c) Hereditary optic neuropathies
I
6) Pituitary adenoma
Pituitary adenoma
Key Objectives
• Determine whether the loss of vision is acute or chronic (at times, the loss
of monocular vision is noted incidentally when the other eye is covered so
that a chronic loss presents acutely).
• Perform direct ophthalmoscope examination of the eye.
Determine whether the visual loss is monocular or binocular.
Differentiate causes of visual loss by examination of cornea, lens,
retina, and optic disc.
Determine the presence of a foreign body, abnormal extraocular
musculature or pupillary reflex.
Perform visual acuity and field testing.
List indications for fluorescein angiography.
• Conduct an effective plan of management for a patient with chronic loss of
vision:
475
121 Vomiting, Nausea
Overview
Nausea may occur alone or along with vomiting (powerful ejection of gastric contents),
dyspepsia (see #003C Chronic Recurrent Abdominal Pain), and other gastrointestinal
complaints. Vomiting may be a manifestation of a systemic, central or local problem.
There is a continuum of severity from a minor inconvenience (and accompaniment to
a systemic illness) to a major life-threatening symptom in conditions such as gastric
obstruction. When prolonged or severe, vomiting may be associated with disturbances
of volume, water and electrolyte metabolism that may require correction prior to other
specific treatment.
Causes
1) Gastrointestinal system
a) Stomach
0 Gastroenteritis
0 Postoperative
0 Acid peptic disease
Gastroparesis I Obstruction
0 Gastro-oesophageal reflux, pyloric or duodenal stenosis
b) Small bowel I Colon
0 Obstruction
0 Acid peptic disease
0 Appendicitis
c) Hepato-biliary disease
d) Pancreatic disease
e) Peritoneal irritation
I 2) Central nervous system (CNS)

a) Infections
b) Tumours
c) Multiple sclerosis
d) Vestibular nerve lesions
e) Brain stem lesions
f) Migraine
g) Psychiatric/Psychologic problems
h) Travel sickness
476
3) Endocrine-metabolic (diabetes, uraemia,
hypercalcaemia, pregnancy)
4) Cancer (paraneoplastic syndromes, ovarian,

hypernephroma, gastric)
I 5) Systemic
a) Sepsis (pyelonephritis, pneumonia, any infection in childhood)
b) Drugs (chemotherapy)
c) Food poisoning
d) Alcohol intoxication
Key Objectives
• Contrast vomiting and regurgitation, which is return of oesophageal
contents into the hypo-pharynx with little effort, such as with gastro-
oesophageal reflux.
• Determine severity of volume and electrolyte abnormalities in a patient
with vomiting.
Determine whether there is a secondary cause for the vomiting,
delayed gastric emptying is present, or the vomiting is in response to
other agents.
Select patients requiring investigation since laboratory testing may be
unnecessary in many.
Select patients in need of endoscopic examination.
• Conduct an effective plan of management for a patient with vomiting and
nausea:
Outline management plan for patients with vomiting caused by
documented diseases, as contrasted to delayed gastric emptying, or
other causes (e.g. chemotherapeutic drugs).
Calculate volume and electrolyte deficit and outline management
(see #0058 Metabolic Alkalosis and #008A Hypokalaemia).
477
122 Weakness/Paralysis/Paresis
Overview
Many patients who complain of weakness are not objectively weak when muscle
strength is formally tested. A careful history and physical examination will permit the
distinction between functional disease and true muscle weakness.
Causes
(see #038 Fatigue)
11) Myopathies
a) Genetic (e.g. muscular dystrophy)
b) Inflammatory (e.g. polymyositis, vasculitis, collagen-vascular)
c) Infectious (e.g. HIV, influenza, cytomegalovirus (CMV))
d) Neoplastic (e.g. malignancy-associated myositis)
e) Toxic/Drug (e.g. steroids, 3-hydroxy-3-methylglutaryl coenzyme A
(HMG-CoA) reductase inhibitors, alcohol)
f) Metabolic/Endocrine (e.g. hypothyroidism, Cushing syndrome,
electrolyte disorders)
12) Neuromuscular junction

a) Genetic (e.g. myasthenia gravis)
b) Inflammatory (e.g. myasthenia gravis)
c) Infectious (e.g. botulism)
d) Neoplastic (e.g. Eaton-Lambert syndrome)
e) Toxic/Drug (e.g. organophosphate poisoning)
13) Peripheral neuropathies

a) Genetic (e.g. peroneal muscular atrophy)
b) Inflammatory (e.g. Guillain-Barre syndrome)
c) Infectious (e.g. leprosy)
d) Neoplastic (e.g. myeloma/amyloid)
e) Toxic/Drug (e.g. lead)
f) Metabolic/Endocrine (e.g. diabetes mellitus)
g) Idiopathic (e.g. Bell palsy)
478
Bell palsy - lower motor neurone
I 4) Anterior horn cell

a) Genetic (e.g. spinal muscular atrophy)
b) Inflammatory (e.g. amyotrophic lateral sclerosis)
c) Infectious (e.g. poliomyelitis)
d) Neoplastic (e.g. paraneoplastic syndromes)
e) Toxic/Drugs (e.g. lead)
I5) Upper motor neuron

a) Genetic (e.g.leucodystrophy)
b) Inflammatory (e.g. vasculitis)
c) Infectious (e.g. brain abscess)
d) Neoplastic (e.g. brain tumour)
e) Toxic/Drug (e.g. radiation)
f) Metabolic/Endocrine (e.g. vitamin 8 , 2 deficiency)
I 6) Functional
Key Objectives
• Differentiate between patients who complain of generalised weakness
(usually functional) compared to patients who complain of inability to
perform specific tasks.
• Differentiate between weakness due to an upper motor neuron lesion and
weakness due to a disturbance affecting the lower motor neuron or motor
unit.
• Determine the cause of the lesion.
479
Determine whether the weakness is localised or generalised, assess
muscle strength, tone, bulk/atrophy, fasciculation , tremor, myoclonus,
tendon reflexes, and plantar reflexes.
Determine whether the weakness occurred as a result of an
abnormality in the cerebral cortex, descending motor pathways, brain
stem, spinal cord , anterior horn cells, nerve roots and plexuses,
peripheral nerves, neuromuscular junction, or skeletal muscle.
List the physiologic principles and indications for electromyelography
(EMG), muscle enzymes.
List indications for muscle biopsy.
• Conduct an effective plan of management for a patient with weakness ,
paresis, or paralysis:
Outline an initial plan of management for Guillain-Barre syndrome.
Outline an initial plan of management for myasthenia gravis.
Outline an initial plan for rehabilitation of patients with hemiplegia and
paraplegia.
480
123 Weight (Low) at Birth I Intra-uterine Growth
Aberration
Overview
Intra-uterine growth restriction (IUGR) is often a manifestation of congenital infections,
poor maternal nutrition or maternal illness. In other patients, the infant may be large for
the gestational age. There may be long term sequelae for both.
Causes
1) Newborn infant small for gestational age (growth restricted)
a) Maternal
0 Social and/or economic status
0 Drugs (cigarettes, alcohol, narcotics, cocaine)
0 Illness (pregnancy-induced hypertension I 'HELLP' (.t:faemolysis,
Elevated L iver enzymes, Low Platelets) syndrome, diabetes,
malnutrition, systemic lupus erythematosus (SLE), lupus
anticoagulant)
b) Fetal
0 Multiple gestation
0 Intra-uterine infections ('TORCH' - Ioxoplasmosis, Qther, Rubella,
Cytomegalovirus, Herpes simplex virus)
0 Chromosomal abnormality
c) Placental insufficiency - infarction, previous placental abruption
2) Newborn infant large for gestational age

a) Maternal (familial, diabetes)
b) Fetal (e.g. Beckwith syndrome, transposition of great vessels)
Key Objective
• Determine the most probable diagnosis by clinical means.
List indications for investigations such as fetal ultrasound , and blood
biochemistry.
481
• Conduct an effective initial plan of management for an infant with intra-
uterine growth aberration:
Discuss the complications associated with IUGR and outline the
management of such an infant.
Outline management and complications that can occur in large-for-
gestational-age infants.
Outline preventive strategies of large-for-gestational-age infants.
• Outline the management in late pregnancy when IUGR or fetal
macrosomia has been diagnosed; including fetal assessment, mode of
delivery and potential problems in labour and at delivery.
482
124 Weight Gain I Obesity
Overview
Obesity is a chronic condition that is increasing in prevalence. It is contributed to by
lifestyle changes including inactivity and dietary changes, and may result in diabetes,
hypertension, atherosclerosis and sleep-apnoea.
Causes
l1) Increased energy intake
a) Dietary (progressive hyperphagic, frequent eating, high-fat diet,
overeating)
b) Social and behavioural (socio-economic, ethnicity, psychological)
c) Iatrogenic (drugs, hormones, hypothalamic surgery)
2) Decreased energy expenditure (sedentary lifestyle, smoking

cessation)
13) Neuroendocrine
a) Hypothyroidism
b) Cushing syndrome
c) Hypothalamic syndrome
d) Polycystic ovary syndrome
e) Hypogonadism
f) Growth hormone (GH) deficiency
Cushing syndrome
14) Genetic (dysmorphic)
483
Key Objectives
• Recognise that the sequelae of obesity may be life-threatening.
• Determine whether obesity is the result of lifestyle changes or
neuroendocrine disorder.
General/Specific ObJectives
Determine the degree and type of obesity.
Determine whether a treatable cause of obesity (secondary or
neuroendocrine) is present.
Describe the risk of morbidity and mortality.
Perform a measurement of waist-to-hip ratio and determine body-mass
index (BMI).
Determine whether comorbid conditions are present (hypertension,
diabetes mellitus, dyslipidaemia, sleep-apnoea, etc.).
Select patients who require investigation for a neuroendocrine cause
of obesity.
• Conduct an effective plan of management for a patient with weight gain I
obesity:
Formulate a plan of management consistent with the reality that the
great majority of patients require chronic long term treatment since
obesity cannot be cured.
List the modalities of treatment for obesity including increased energy
expenditure through exercise, decreased energy intake through
healthy diets, and behaviour modification.
Contrast advantages and disadvantages of anorectic drugs and
surgery for the treatment of obesity.
484
125 Weight Loss I Eating Disorders I Anorexia I
Nutritional Disorders
125A Weight Loss I Eating Disorders I Anorexia
Overview
Involuntary weight loss is nearly always a sign of serious medical or psychiatric illness
and should be investigated.
Causes
11) Involuntary weight loss
a) Decreased energy intake
0 Malignancy decreasing appetite
0 HIV
0 Endocrinopathies (adrenal insufficiency, hypercalcaemia, diabetes
mellitus)
0 Chronic illness (chronic obstructive pulmonary disease (COPD),
congestive cardiac failure (CCF))
0 Gastrointestinal disease (obstruction and malabsorption)
0 Intercurrent illness (hepatitis, glandular fever, chronic fatigue
syndrome)
0 Psychiatric disease (bipolar disorder, personality disorder, paranoia/
delusion)
0 Drugs (alcohol, opiates, cocaine , amphetamines, anticancer)
b) Increased energy expenditure
0 Hyperthyroidism
0 Phaeochromocytoma
0 Chronic illness (COPD, CCF)
0 Malignancy (hypercatabolic)
0 Infection (presence of fever indicative of hypercatabolic state)
c) Energy loss
0 Urine (uncontrolled diabetes mellitus)
0 Stool (malabsorption)
12) Voluntary weight loss

a) Decreased intake
0 Diet for treatment of obesity
0 Anorexic drugs
0 Anorexia I Bulimia
0 Psychological
b) Increased energy expenditure (distance runners, models, ballet
dancers, gymnasts)
485
Key Objectives
• Determine extent of weight loss in relation to previous weight, whether
voluntary or involuntary, whether with increased appetite or decreased
appetite, and if fluctuations in weight are usual or unusual. l
Differentiate involuntary weight loss from voluntary.
Contrast weight loss associated with increased appetite from that with
decreased appetite.
Conduct an investigation of involuntary weight loss, whether appetite is
decreased or increased.
• Conduct an effective plan of management for a patient with weight loss I
eating disorder I anorexia:
State that management is dependent on the underlying condition.
Counsel patients with voluntary weight loss on healthy diets and
lifestyle changes.
486
125 Weight Loss I Eating Disorders I Anorexia I
Nutritional Disorders
1258 Nutritional Disorders and Deficiencies
Overview
No clinical assessment is entirely complete without an assessment of the patient's
nutritional status. Nutritional disorders present from infancy through to old age. They
may involve disorders of energy-yielding macronutrients (carbohydrate/fat/protein) or
of essential organic/inorganic micronutrients (vitamins I trace elements).
Serious illness, prolonged hospitalisation and inanition are likely to be associated
with varying degrees of protein-energy malnutrnion (PEM) from negative energy
balance, particularly in the presence of uncontrolled chronic sepsis.
Vitamin and trace element deficiencies cause syndromes relating to thei r specific
metabolic effects. For example zinc, a predominantly intracellular cation , is a
component of important enzyme systems involved in active cellular proliferation and
repair. Zinc deficiency gives clinical manifestations which include an exanthematous
rash , gastrointestinal symptoms, and problems with wound healing.
Causes of Nutritional Deficiencies

11) Energy-yielding macronutrients
a) PEM (undernutrition, starvation, marasmus/kwashiorkor)
I2) Inorganic nutrients

a) Calcium and phosphorous
(see also #004 Abnormal Serum Calcium/Phosphate, #064 Menopause
and #077 Periodic Health Examination I Growth and Development)
b) Iron
(see also #012 Anaemia and Pallor)
c) Iodine
(see also #068 Neck or Facial Mass I Goitre I Thyroid Disease)
d) Zinc and other trace elements (zinc, manganese, beryllium, boron,
selenium, cobalt, etc.)
day 0 day 2 day 7

Zinc deficl6ncy - replacement therapy
487
I 3) Organic nutrients
a) Fat-soluble vitamins (A, D, E, K)
b) Water-soluble vitam ins (B complex, C)
Rickets
Key Objectives
• Identify those patients liable to develop syndromes of nutritional
deficiencies.
• Recognise clinical features of major deficiencies.
Conduct a clinical assessment of nutritional status from history,
physical examination and appropriate office tests.
Diagnose syndromes of PEM; compare and contrast features
applicable to children and to adults.
Appreciate principles of normal energy balance and of dietary
requirements of major energy sources.
Appreciate principles of micronutrient requirements.
Appreciate risk factors for nutritional depletions and institute preventive
measures where appropriate.
Diagnose trace element and vitamin deficiencies in patients at risk.
• Select appropriate investigations which were key in the processes of
exclusion, differentiation and diagnosis, recognising that serum or urinary
measurements of vitamins and trace elements are not routinely done and
may not be available or diagnostically helpful at short notice.
• Outline effective plans of management for patients with PEM , vitamin
deficiency or trace element deficiencies:
Outline basal requirements of energy intake and expenditure
(kilojoules/calories) and daily requirements and proportions of
macronutrients and essential micronutrients.
Outline methods and principles of formulation of enteral and parenteral
nutrition regimens.
Discuss complications and hazards of parenteral nutrition.
488
126 Wheezing I Respiratory Difficulty I Stridor
126A Upper Respiratory Tract Disorders
Overview
Wheezing, a whistling sound, is produced by vibration of opposing walls of an airway
that is narrowed almost to the point of closure. It can originate from airways of any size,
from upper airways to intrathoracic small airways. Stridor is an even more strident,
urgent, harsh noise indicating extreme difficulty with breathing.
Causes
1) Extrathoracic upper airway obstruction
a) Sleep-apnoea syndrome I Obesity
b) Goitre
c) Postnasal drip
d) Vocal cord dysfunction (nodule, paresis)
e) Epiglottitis
f) Laryngeal oedema/stenosis
g) Anaphylaxis
h) Retropharyngeal mass (abscess, neoplasm)
Retrostemal goitre extension causing stridor
4B9
2) Intrathoracic upper airway obstruction
a) Tracheobronchitis
b) Tracheal obstruction (stenosis, compression, e.g. retrosternal thyroid
mass)
c) Foreign body aspiration
d) Tracheal or bronchial tumours (benign, malignant)
Key Objectives
• Determine whether the wheezing is associated with chronic dyspnoea and
cough, because this triad is highly suggestive of asthma.
• Appreciate that asthma is not the sole or most common cause of
wheezing; identify extrathoracic/intrathoracic upper airway obstruction
(e.g. from thyroid}.
Determine whether the wheezing is polyphonic, since if so it is more
likely to originate from more central airways.
Determine if wheezing is maximum in inspiration or expiration, and
whether accompanied by stridor.
Determine the most likely site of obstruction, whether large or small
intrathoracic airway or extrathoracic airway.
From history and clinical examination, determine the most likely cause
and the urgency of management.
List indications for diagnostic imaging.
Select pulmonary function studies as one means to differentiate
between causes once diagnostic possibilities have been narrowed by
clinical means.
• Conduct an effective plan of management for a patient with upper
respiratory tract disorders:
Outline the use of bronchodilator therapy for diagnostic purposes.
490
-
126 Wheezing I Respiratory Difficulty I Stridor
1268 Lower Respiratory Tract Disorders
Overview
Individuals with episodes of wheezing , breathlessness, chest tightness, and cough
usually have limitation of airflow. The most common cause of airflow limitation is
asthma which is reversible with treatment. Without treatment it may be lethal.
While the prevalence of asthma is rising (asthma affects an estimated 2,000,000
Australians) , the mortality from asthma has fallen dramatically - deaths in Australia
yearly have decreased from around 1,200 a decade ago to around 400 cu rrently.
Causes
11) Obstructive lung disease
a) Asthma
b) Chronic obstructive pulmonary disease (COPD)
c) Bronchiectasis
d) Cystic fibrosis
12) Small airway disorder

a) Aspiration
b) Bronchiolitis
c) Cystic fibrosis
13) Cardiovascular
a) Pulmonary oedema
b) Pulmonary embolism
Key Objectives
• Determine the severity of the airway obstruction and use this to guide
therapy.
• Distinguish respiratory and cardiac causes of respiratory symptoms.
491
Elicit information about intermittency, seasonal waxing and waning ,
nocturnal episodes, exacerbation on exposure to exercise, cold air,
allergens, air pollutants, or upper respiratory tract infections (URTis)
(suggestive of asthma, but also found in COPD and bronchiectasis).
Determine whether the wheezing is polyphasic (multiple pitches, start
and stop at various points in respiratory cycle).
Examine and discuss evaluation of sputum.
Understand that pulmonary function tests are key to diagnosis and
management of asthma. Select spirometry and FEV1 (forced expiratory
vital capacity in one second) before and after bronchodilator inhalation,
to quantify severity of airway narrowing and to define reversibility.
Discuss the use of provocative testing for diagnosis of asthma if lung
function is normal.
Select diagnostic imaging to detect complications of asthma and to
exclude alternative diagnoses.
List indications for allergy testing for asthma.
• Conduct an effective plan of management for a patient with lower
respiratory tract disorders:
Outline an initial plan of management for a patient with asthma.
492
127 Allergic Reactions
Overview
Allergic reactions are common in all age groups. They exhibit a variety of clinical
responses and are considered individually elsewhere under the appropriate
presentation. The rationale for considering them together is that in some patients with
one response (e.g. atopic dermatitis), other atopic disorders such as asthma or allergic
rhinitis may occur at other times. Moreover, 50% of patients with atopic dermatitis
report a family history of respiratory atopy. The child of a mother with atopy is at high
risk for atopic diseases.
Clinical Presentations
1) Allergic rhinitis, rhinorrhoea, hay fever
(see #092 Rhinorrhoea I Sore Throat)
I 2) Eye redness
(see #035 Eye Redness)
13) Anaphylaxis
(see #098A Anaphylaxis)
I 4) Skin rash I Dermatitis

(see #1 02A Skin Rash I Dermatitis and/or Fever, Urticaria/Angie-Oedema)
Allergic rash
493
Is) Urticaria/Angio-oedema
(see #1 02A Skin Rash I Dermatitis and/or Fever, Urticaria/Angie-Oedema)
Allergic periorbital oedema
I6) Atopic dermatitis

(see #102A Skin Rash I Dermatitis and/or Fever, Urticaria/Angie-Oedema)
Flexural atopic dermatitis
j 7) Wheezing I Respiratory difficulty

(see #126A Upper Respiratory Tract Disorders and #1268 Lower Respiratory
Tract Disorders)
Key Objectives
• Recognise allergy as the probable basis of a variety of cli nical
presentations.
• Familiarity with common allergens.
• Diagnose potentially lethal anaphylaxis and initiate immediate treatment.
494
Elicit a history or identify the possible causes of an anaphylactic
reaction .
Differentiate between food intolerance and food allergy.
Identify common allergens and their possible effects on susceptible
individuals.
List cost-effective use of tests designed to identify allergens.
Interpret results so as to differentiate the allergic from the non-allergic
individual.
• Conduct an effective plan of management for a patient with allergies:
Outline emergency management of anaphylaxis, with and without
shock.
Discuss skin testing in allergic patients.
Outline the immediate and long term management of the child with
allergies including education and counselling for the child, parents,
school and the community.
Identify the social and psychologic impact of allergic disease on the
child and its family.
495
128 Bites, Stings and Envenomations
Overview
Bites and stings in Australia from land, air and marine creatures are commonplace but
serious and fatal bites are uncommon. Knowledge of first aid measures and early
treatment is required for all clinicians; effective first aid using the pressure-
immobilisation technique lowers risks of envenomation and can be life-saving.
Polyvalent and specific anti-venoms are available for most snake, spider and marine
bites and stings and have significantly reduced mortality and morbidity.
Fatalities from predators such as crocodiles and sharks are horrifying and invoke
headlines, but are rare compared to other causes of death. In a 10-year period
between 1980 and 1990, in rounded figures there were 5 fatal crocodile and 10 fatal
shark attacks in Australia. In the same period, 20 people died from bee stings, 20
people were fatally struck by lightning, 3,000 people drowned and 30,000 people
died in accidents involving motor vehicles.
Causes
1) Snake bites
Venomous Australian snakes include taipan and small-scaled snake, tiger
snake, brown and black snakes, copperhead, death adder and others. The
comparative lethal effects in mice of small-scaled snake ('fierce snake') venom
is 50 times greater than Indian king cobra venom and 1,000 times greater than
American rattlesnake venom.
Tiger snake
I2) Spider bites

Toxins of a few species (funnel-web, red-back) can cause severe systemic and
local symptoms, and deaths from envenomation can occur. Painful necrotising
arachnidism is a feature of some species (white-tailed spider, wolf spider).
Most species evoke local pain and inflammation only.
496
I 3) Marine bites, stings and attacks
a) Sandfly bites:
These are the most common beach irritant.
b) Blue-ringed octopus and cone shell venoms:
These can cause respiratory paralysis.
c) Stonefish, scorpion fish and stingray:
These have venomous spines and injuries can cause intense pain.
d) Box jellyfish ( Chironex fleckeri- 'seawasp'):
Stings can occur in northern coast areas in summer and are intensely
painful; occasional fatalities have occurred.
e) Other northern jellyfish carybdeid species (' lrukandji' syndrome:
Carukia barnes1):
These can cause severe systemic effects and hypertension.
f) 'Bluebottle', and other jellyfish species
g) Attacks by estuarine crocodiles and sharks:
These can cause gross wounding and death.
LHCh bite
487
I 4) Other Bites and Stings
a) Ticks (Australian paralysis t ick- 'bush tick': Ixodes holocyclus)
b) Ants, bees, wasps, mosquitoes, scorpions, caterpillars, leeches
c) Domestic animals (dog and cat bites, etc.)
d) Human bite injuries
Infected human bite wound
Key Objectives
• Appreciate principles of first aid management for bites and stings by
pressure-immobilisation, and of local management of the wound for
specific causes.
• Recognise symptoms of envenomation and institute treatment.
• Construct an algorithm for management of a bite from an unidentified
snake.
• Describe principles of local and general treatment of stings from :
A bee.
A wasp.
A box jellyfish.
A funnel-web spider.
An unidentified spider bite.
• Demonstrate the technique of effective pressure-immobilisation for a
snake bite to a limb.
4st8
129 Deformities/Malformations
129A Congenital Malformations
(See also #043 Genetic Concerns, Dysmorphic Fe atures)
Overview
Management of malformations is a very important component of paediatric care. Some
of the more common conditions encountered in Australia are summarised here. Many
will also have been discussed in relation to specific conditions. No system is exempt
from either single or multiple malformation. Causes include exogenous teratogens,
chromosomal abnormalities, and an abnormal dominant or recessive gene; but in
most instances the cause is unknown. Incidence of inguinal hernia in liveborn children
is approximately 1:70; of more serious lesions such as trachea-oesophageal fistula
approximately 1:5,000.
Predisposing Causal Factors

These include parental age, consanguinity, race, maternal diseases, birth rank and
sex of child.
Common Malformations:
11) Cleft lip and palate
I 2) Umbilical or inguinal hernia
13) Club foot (talipes)
4) Developmental dysplasia of hip (DDH, CDH)
Bilateral developmentsJ dysplasia

of hips
488
Is) Scoliosis
16) Syndactyly, polydactyly, camptodactyly
I 7) Phocomelia
8) Thyroglossal cyst, branchial cyst/sinus,

lymphatic maHormation
Lymphatic malfonnatlon
I 9) Congenital heart disease
1 10) Tracheo-oesophageal fistula
T~flstula
11) Diaphragmatic hernia
12) Myelomeningocele
500
13) Hydrocephalus
14) Urinary tract anomalies
15) Anal atresia
16) Exomphalos
17) Hypospadias
18) Ambiguous genitalia
Precipitating Teratogens:
11) Physical (ionising radiation)
2) Chemical/Pharmacological (thalidomide,
folic acid antagonists, etc.)
I 3) Infections (rubella, etc.)
I 4) Dietary deficiency (goitre)
Key Objectives
• Be able to advise about known preventive factors, especially
periconceptual folate in prevention of neural tube defects.
• As well as preventive measures:
Diagnose malformations as early as possible after birth.
• Provide empathetic counselling and appropriate referral.
501
/
129 Deformities/Malformations ·
1298 Hand Deformities
Overview
Structural abnormalities and deformities in adults are common consequences of disease
of bones or soft tissues; many are described with the relevant causative cond ition.
The more common hand deformities are grouped as an illustrative example.
Causes
11) Congenital contractures
a) Congenital contracture of little finger (camptodactyly, clinodactyly -
approximately 1 :200 incidence)
Camptodactyly
2) Dupuytren disease (nodule, contractures- palmar fasciae)
I 3) Muscle contracture
a) Long flexor forearm muscles (Volkmann ischaemic contracture)
b) Short hand muscles ('intrinsic plus' deformity - rheumatoid arthritis
(RA), cerebral palsy hypertonicity)
I 4) Tendon deformities
a) Trigger finger (stenosing tenosynovitis)
b) Mallet finger
c) Boutonniere deformity
d) Swan neck deformity
e) Spontaneous tendon rupture (dropped finger, thumb)
502
Dupuytren contracture
I 5) Bone and joint deformities

a) Osteoarthritis
0 Distal interphalangeal joints (Heberden nodes)
Proximal interphalangeal joints (Bouchard nodes)
Carpo-metacarpal joint of thumb
b) RA
0 Wrist deformity, metacarpo-phalangeal joint subluxations, ulnar
deviation fingers, Z-thumb deformity, etc.
c) Gout - tophaceous arthropathy
Heberden nodes
503
I 6) Neurological deformities
a) Radial or posterior interosseous nerve- wrist and finger drop
b) Ulnar nerve palsy- ulnar claw hand
c) Median nerve palsy- 'simian' hand, 'accoucheur' hand, pseudo-
opposition
d) Upper brachial plexus lesion (CS, C6 nerve roots- Erb paralysis)
e) Lower brachial plexus lesion (T1 nerve root- Klumpke paralysis
(complete claw hand))
f) Others (syringomyelia, leprosy, motor neurone disease, poliomyelitis
- variants of claw hand)
Key Objective
• Diagnose individual deformities and causative conditions from careful
history and physical examination.
Appreciate mechanisms of deformity resulting from individual causes.
Differentiate fixed from mobile deformities.
Conduct focused examination of hand status, and assess effect of
deformities on hand function.
Discuss appropriate medical and surgical methods for correcting/
coping with individual deformities.
504
130 Travel Medicine and Tropical Infections
Overview
A number of tropical infections is prevalent in the Australian Far North.
Additionally, international air travel and tourism have faci litated the spread of infectious
diseases worldwide; and the potential spectre of bio-terrorism is relevant to all countries.
All medical practitioners require basic knowledge of diseases not normally native to
their own country, including those likely to cause fatal epidemics.
Travellers are exposed to the ubiquitous risks of traveller's diarrhoea, to diseases
prevalent in the visited countries, and to sexually transmitted diseases (STDs) including
AIDS .
Causes
1) Tropical and specific fevers
a) Brucellosis (Brucella abortus)
b) Q fever (Coxiella burnetii)
c) Malaria (Plasmodium falciparum, etc.)
d) Dengue (arbovirus)
e) Amoebiasis (Entamoeba histolytica)
f) Melioidosis (Pseudomonas pseudomalle1)
g) Leptospirosis (Leptospira pomona)
h) Ross River fever (arbovirus)
i) Murray Valley encephalitis (arbovirus)
j) Listeriosis (Listeria monocytogenes)
2) Zoonoses/Ornithoses (infections transmitted between

animals or birds and humans)
a) Bovine tuberculosis (TB), brucellosis, listeriosis, Lyme disease,
plague, psittacosis, rabies, typhus, etc.
b) Schistosomiasis (bilharziasis) I Trypanosomiasis
I 3) Biological agents as weapons

a) Anthrax (Bacillus anthracis)
b) Plague ( Yersinia pestis)
505
Key Objectives
• Ability to advise on risks and precautions of overseas travel.
• Awareness of endemic Australian infectious diseases and fevers.
• Awareness of potential for exotic illness and epidemics.
General/Specific Objective
• Outline reference sources and recommended immunisations and
precautions for overseas travellers visiting Asian , European, North and
South American countries.
506
131 Medical Emergencies
131A Life-Threatening Emergencies
(See also #019 Cardiac Arrest 1 Respiratory Arrest)
Overview
Life-threatening medical emergencies requi re early recognition and prompt treatment
to avert death. Treatment and diagnostic plans must proceed simultaneously and
rapidly if success is to be achieved. Competence in dealing with primary care of each
of the following emergencies is a basic cl inical skills requirement for all medical
practitioners. Most are also dealt with under headings of the causal conditions. Some
of the most seriously life-threatening causes of medical emergencies are grouped
below.
Causes
1) Cardiac emergencies
a) Cardiac arrest
b) Cardiac dysrhythmias
c) Acute cardiac failure
d) Acute pericardia! tamponade
2) Ventilatory/Respiratory emergencies
a) Respiratory arrest
b) Airway obstruction I Asphyxiation
c) Tension pneumothorax
d) Flail chest
I3) Circulatory emergencies

a) Haemorrhage
0 Overt/Concealed
0 Primary I Reactionary I Secondary
0 Arterial/Venous/Capillary
b) Shock
0 Hypovolaemic
0 Cardiac
0 Obstructive (thromboembolism, air embolism, tamponade)
0 Septic
0 Anaphylactic
507
4) Overwhelming sepsis (e.g. meningoc occal septicaem!a)
Is) Cerebral emergencies

a) Disturbed consciousness
U Coma/Stupor (meningitis/encephalitis, traumatic cerebral
compression)
(J Acute brain syndrome (delirium)
b) Convulsions/Seizures
16) Multisystem/Organ failure

a) Acute renal failure (ARF) (oliguric/nonoliguric) with severe
hyperkalaemia
b) Acute haematologic failure (disseminated intravascular coagulation
(DIC)) with massive bleeding
c) Acute gastrointestinal failure (stress ulcer syndrome/necrotising
enteritis) with massive bleeding or peritonitis
d) Acute metabolic emergencies (acid-base disequilibrium, water-
electrolyte disturbance)
17) Drowning/Electrocution
Key Objectives
• Demonstrate competence in primary care of medical emergencies.
• Recognise life-threatening medical emergencies and their causes as early
as possible.
• Appreciate principles and practice of combined therapeutic and diagnostic
plans for initial management of such emergencies.
• Appreciate the specific treatment and diagnostic plans for individual
emergencies.
• Construct algorithms to deal efficaciously with each emergency, including
specific diagnostic tests.
508

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001 Abdominal Distension/Ileus (Ascites, Bowel

j 1) Acute abdominal distension

Abdominal distension- pyloric stenosis (adult)

b) Non-mechanical intestinal obstruction

Abdominal distension - ascites

3) Chronic nonmechanical intestinal pseudo-obstruction

12) Gastrointestinal system masses

3) Vascular (abdominal aortic aneurysm)

14) Gynaecologic J Pelvic Retroperitoneal liposarcoma

I6) Masses in abdominal wall

002A Epigastric Mass

2) Gastric mass (neoplasm, gastric dilatation)

13) Liver mass (left lobe)

4) Pancreatic mass (pseudocyst, tumour)

Is) Lymph node mass (para-aortic nodes)

0028 Right Hypochondria/ Mass

12) Enlarged gallbladder

13) Hepatic flexure colonic mass

14) Right renal mass

Daughter cysts In hepatic hydatid

Primary hepatocellular carcinoma

002C Left Hypochondria/ Mass

2) Left renal mass

3) Colonic mass (splenic flexure)

4) Pancreatic tail mass

0020 Right Iliac Fossa Mass

12) Caecal mass (carcinoma)

14) Iliac lymph node swellings

002E Suprapubic/Pelvic Mass

Suprapubic/pelvic mass - ovarian cyst

002F Left Iliac Fossa Mass

I 2) Lymph node mass

002G Abdominal Hernia

l1) Groin hernias

I2) Umbilical hernias

13) lncisional (wound) hernia

b) Wound infection commonest cause

14) Less common abdominal wall hernias!

Bilateral inguinal hernias

a) Diffuse epigastric bulge between recti in epigastrium due to obesity

6) Internal abdominal hernias

002H Adrenal Mass

11) Non-functioning ade noma

I2) Functioning ade noma

I 5) Ne uroblastoma (in children) I

Adrenal mass on CT, with serum chemistry - Conn syndrome

003A Abdominal Pain in Adults

I 3) Left upper quadrant pain

6) Special group 'acute abdomen - acute abdominal surgical

Perforated colonic diverticulitis Intestinal obstruction - stangulated

0038 Non-Acute/Recurrent Abdominal Pain in Infancy

003C Chronic Recurrent Abdominal Pain

I2) Relat ed organs

Bile duct stone - MRCP and ERCP

2) Gastro-oesophageal reflux disease with/without oesophagitis

I3) Motility disorders of the oesophagus

4) Peptic ulcer disease (including drugs)

5) Miscellaneous (biliary disease, irritable bowel, chronic

Oesophageal motility disorder

Sliding oesophageal hiatus hernia

003E Anal Pain

003F Acute Abdominal Pain in Children

Inguinal hernia - non-reducible Ileocolic intussusception